---
_id: '1142'
abstract:
- lang: eng
text: Hemolysis drives susceptibility to bacterial infections and predicts poor
outcome from sepsis. These detrimental effects are commonly considered to be a
consequence of heme-iron serving as a nutrient for bacteria. We employed a Gram-negative
sepsis model and found that elevated heme levels impaired the control of bacterial
proliferation independently of heme-iron acquisition by pathogens. Heme strongly
inhibited phagocytosis and the migration of human and mouse phagocytes by disrupting
actin cytoskeletal dynamics via activation of the GTP-binding Rho family protein
Cdc42 by the guanine nucleotide exchange factor DOCK8. A chemical screening approach
revealed that quinine effectively prevented heme effects on the cytoskeleton,
restored phagocytosis and improved survival in sepsis. These mechanistic insights
provide potential therapeutic targets for patients with sepsis or hemolytic disorders.
acknowledgement: 'Y. Fukui (Medical Institute of Bioregulation, Kyushu University)
and J. Stein (Theodor Kocher Institute, University of Bern) are acknowledged for
providing the DOCK8 deficient bone marrow. and H. Häcker (St. Judes Children''s
Research Hospital) for providing the ERHBD-HoxB8-encoding retroviral construct.
pSpCas9(BB)-2a-Puro (PX459) was a gift from F. Zhang (Massachusetts Institute of
Technology) (Addgene plasmid # 48139) and pGRG36 was a gift from N. Craig (Johns
Hopkins University School of Medicine) (Addgene plasmid # 16666). LifeAct-GFP-encoding
retrovirus was kindly provided by A. Leithner (Institute of Science and Technology
Austria). pSIM8 and TKC E. coli were gifts from D.L. Court (Center for Cancer Research,
National Cancer Institute). We acknowledge M. Gröger and S. Rauscher for excellent
technical support (Core imaging facility, Medical University of Vienna). We thank
D.P. Barlow and L.R. Cheever for critical reading of the manuscript. This work was
supported by the Austrian Academy of Sciences, the Science Fund of the Austrian
National Bank (14107) and the Austrian Science Fund FWF (I1620-B22) in the Infect-ERA
framework (to S.Knapp).'
author:
- first_name: Rui
full_name: Martins, Rui
last_name: Martins
- first_name: Julia
full_name: Maier, Julia
last_name: Maier
- first_name: Anna
full_name: Gorki, Anna
last_name: Gorki
- first_name: Kilian
full_name: Huber, Kilian
last_name: Huber
- first_name: Omar
full_name: Sharif, Omar
last_name: Sharif
- first_name: Philipp
full_name: Starkl, Philipp
last_name: Starkl
- first_name: Simona
full_name: Saluzzo, Simona
last_name: Saluzzo
- first_name: Federica
full_name: Quattrone, Federica
last_name: Quattrone
- first_name: Riem
full_name: Gawish, Riem
last_name: Gawish
- first_name: Karin
full_name: Lakovits, Karin
last_name: Lakovits
- first_name: Michael
full_name: Aichinger, Michael
last_name: Aichinger
- first_name: Branka
full_name: Radic Sarikas, Branka
last_name: Radic Sarikas
- first_name: Charles
full_name: Lardeau, Charles
last_name: Lardeau
- first_name: Anastasiya
full_name: Hladik, Anastasiya
last_name: Hladik
- first_name: Ana
full_name: Korosec, Ana
last_name: Korosec
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Michelle
full_name: Duggan, Michelle
id: 2EDEA62C-F248-11E8-B48F-1D18A9856A87
last_name: Duggan
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
- first_name: Harald
full_name: Esterbauer, Harald
last_name: Esterbauer
- first_name: Jacques
full_name: Colinge, Jacques
last_name: Colinge
- first_name: Stephanie
full_name: Eisenbarth, Stephanie
last_name: Eisenbarth
- first_name: Thomas
full_name: Decker, Thomas
last_name: Decker
- first_name: Keiryn
full_name: Bennett, Keiryn
last_name: Bennett
- first_name: Stefan
full_name: Kubicek, Stefan
last_name: Kubicek
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Giulio
full_name: Superti Furga, Giulio
last_name: Superti Furga
- first_name: Sylvia
full_name: Knapp, Sylvia
last_name: Knapp
citation:
ama: Martins R, Maier J, Gorki A, et al. Heme drives hemolysis-induced susceptibility
to infection via disruption of phagocyte functions. Nature Immunology.
2016;17(12):1361-1372. doi:10.1038/ni.3590
apa: Martins, R., Maier, J., Gorki, A., Huber, K., Sharif, O., Starkl, P., … Knapp,
S. (2016). Heme drives hemolysis-induced susceptibility to infection via disruption
of phagocyte functions. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3590
chicago: Martins, Rui, Julia Maier, Anna Gorki, Kilian Huber, Omar Sharif, Philipp
Starkl, Simona Saluzzo, et al. “Heme Drives Hemolysis-Induced Susceptibility to
Infection via Disruption of Phagocyte Functions.” Nature Immunology. Nature
Publishing Group, 2016. https://doi.org/10.1038/ni.3590.
ieee: R. Martins et al., “Heme drives hemolysis-induced susceptibility to
infection via disruption of phagocyte functions,” Nature Immunology, vol.
17, no. 12. Nature Publishing Group, pp. 1361–1372, 2016.
ista: Martins R, Maier J, Gorki A, Huber K, Sharif O, Starkl P, Saluzzo S, Quattrone
F, Gawish R, Lakovits K, Aichinger M, Radic Sarikas B, Lardeau C, Hladik A, Korosec
A, Brown M, Vaahtomeri K, Duggan M, Kerjaschki D, Esterbauer H, Colinge J, Eisenbarth
S, Decker T, Bennett K, Kubicek S, Sixt MK, Superti Furga G, Knapp S. 2016. Heme
drives hemolysis-induced susceptibility to infection via disruption of phagocyte
functions. Nature Immunology. 17(12), 1361–1372.
mla: Martins, Rui, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection
via Disruption of Phagocyte Functions.” Nature Immunology, vol. 17, no.
12, Nature Publishing Group, 2016, pp. 1361–72, doi:10.1038/ni.3590.
short: R. Martins, J. Maier, A. Gorki, K. Huber, O. Sharif, P. Starkl, S. Saluzzo,
F. Quattrone, R. Gawish, K. Lakovits, M. Aichinger, B. Radic Sarikas, C. Lardeau,
A. Hladik, A. Korosec, M. Brown, K. Vaahtomeri, M. Duggan, D. Kerjaschki, H. Esterbauer,
J. Colinge, S. Eisenbarth, T. Decker, K. Bennett, S. Kubicek, M.K. Sixt, G. Superti
Furga, S. Knapp, Nature Immunology 17 (2016) 1361–1372.
date_created: 2018-12-11T11:50:22Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2021-01-12T06:48:36Z
day: '01'
department:
- _id: MiSi
- _id: PeJo
doi: 10.1038/ni.3590
intvolume: ' 17'
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d
month: '12'
oa: 1
oa_version: Submitted Version
page: 1361 - 1372
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '6216'
quality_controlled: '1'
scopus_import: 1
status: public
title: Heme drives hemolysis-induced susceptibility to infection via disruption of
phagocyte functions
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 17
year: '2016'
...
---
_id: '1150'
abstract:
- lang: eng
text: When neutrophils infiltrate a site of inflammation, they have to stop at the
right place to exert their effector function. In this issue of Developmental Cell,
Wang et al. (2016) show that neutrophils sense reactive oxygen species via the
TRPM2 channel to arrest migration at their target site. © 2016 Elsevier Inc.
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Renkawitz J, Sixt MK. A Radical Break Restraining Neutrophil Migration. Developmental
Cell. 2016;38(5):448-450. doi:10.1016/j.devcel.2016.08.017
apa: Renkawitz, J., & Sixt, M. K. (2016). A Radical Break Restraining Neutrophil
Migration. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2016.08.017
chicago: Renkawitz, Jörg, and Michael K Sixt. “A Radical Break Restraining Neutrophil
Migration.” Developmental Cell. Cell Press, 2016. https://doi.org/10.1016/j.devcel.2016.08.017.
ieee: J. Renkawitz and M. K. Sixt, “A Radical Break Restraining Neutrophil Migration,”
Developmental Cell, vol. 38, no. 5. Cell Press, pp. 448–450, 2016.
ista: Renkawitz J, Sixt MK. 2016. A Radical Break Restraining Neutrophil Migration.
Developmental Cell. 38(5), 448–450.
mla: Renkawitz, Jörg, and Michael K. Sixt. “A Radical Break Restraining Neutrophil
Migration.” Developmental Cell, vol. 38, no. 5, Cell Press, 2016, pp. 448–50,
doi:10.1016/j.devcel.2016.08.017.
short: J. Renkawitz, M.K. Sixt, Developmental Cell 38 (2016) 448–450.
date_created: 2018-12-11T11:50:25Z
date_published: 2016-09-12T00:00:00Z
date_updated: 2021-01-12T06:48:39Z
day: '12'
department:
- _id: MiSi
doi: 10.1016/j.devcel.2016.08.017
intvolume: ' 38'
issue: '5'
language:
- iso: eng
month: '09'
oa_version: None
page: 448 - 450
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '6208'
quality_controlled: '1'
scopus_import: 1
status: public
title: A Radical Break Restraining Neutrophil Migration
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 38
year: '2016'
...
---
_id: '1154'
abstract:
- lang: eng
text: "Cellular locomotion is a central hallmark of eukaryotic life. It is governed
by cell-extrinsic molecular factors, which can either emerge in the soluble phase
or as immobilized, often adhesive ligands. To encode for direction, every cue
must be present as a spatial or temporal gradient. Here, we developed a microfluidic
chamber that allows measurement of cell migration in combined response to surface
immobilized and soluble molecular gradients. As a proof of principle we study
the response of dendritic cells to their major guidance cues, chemokines. The
majority of data on chemokine gradient sensing is based on in vitro studies employing
soluble gradients. Despite evidence suggesting that in vivo chemokines are often
immobilized to sugar residues, limited information is available how cells respond
to immobilized chemokines. We tracked migration of dendritic cells towards immobilized
gradients of the chemokine CCL21 and varying superimposed soluble gradients of
CCL19. Differential migratory patterns illustrate the potential of our setup to
quantitatively study the competitive response to both types of gradients. Beyond
chemokines our approach is broadly applicable to alternative systems of chemo-
and haptotaxis such as cells migrating along gradients of adhesion receptor ligands
vs. any soluble cue. \r\n"
acknowledgement: 'This work was supported by the Swiss National Science Foundation
(Ambizione fellowship; PZ00P3-154733 to M.M.), the Swiss Multiple Sclerosis Society
(research support to M.M.), a fellowship from the Boehringer Ingelheim Fonds (BIF)
to J.S., the European Research Council (grant ERC GA 281556) and a START award from
the Austrian Science Foundation (FWF) to M.S. #BioimagingFacility'
article_number: '36440'
author:
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Veronika
full_name: Bierbaum, Veronika
id: 3FD04378-F248-11E8-B48F-1D18A9856A87
last_name: Bierbaum
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Tino
full_name: Frank, Tino
last_name: Frank
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Savaş
full_name: Tay, Savaş
last_name: Tay
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Matthias
full_name: Mehling, Matthias
id: 3C23B994-F248-11E8-B48F-1D18A9856A87
last_name: Mehling
orcid: 0000-0001-8599-1226
citation:
ama: Schwarz J, Bierbaum V, Merrin J, et al. A microfluidic device for measuring
cell migration towards substrate bound and soluble chemokine gradients. Scientific
Reports. 2016;6. doi:10.1038/srep36440
apa: Schwarz, J., Bierbaum, V., Merrin, J., Frank, T., Hauschild, R., Bollenbach,
M. T., … Mehling, M. (2016). A microfluidic device for measuring cell migration
towards substrate bound and soluble chemokine gradients. Scientific Reports.
Nature Publishing Group. https://doi.org/10.1038/srep36440
chicago: Schwarz, Jan, Veronika Bierbaum, Jack Merrin, Tino Frank, Robert Hauschild,
Mark Tobias Bollenbach, Savaş Tay, Michael K Sixt, and Matthias Mehling. “A Microfluidic
Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine
Gradients.” Scientific Reports. Nature Publishing Group, 2016. https://doi.org/10.1038/srep36440.
ieee: J. Schwarz et al., “A microfluidic device for measuring cell migration
towards substrate bound and soluble chemokine gradients,” Scientific Reports,
vol. 6. Nature Publishing Group, 2016.
ista: Schwarz J, Bierbaum V, Merrin J, Frank T, Hauschild R, Bollenbach MT, Tay
S, Sixt MK, Mehling M. 2016. A microfluidic device for measuring cell migration
towards substrate bound and soluble chemokine gradients. Scientific Reports. 6,
36440.
mla: Schwarz, Jan, et al. “A Microfluidic Device for Measuring Cell Migration towards
Substrate Bound and Soluble Chemokine Gradients.” Scientific Reports, vol.
6, 36440, Nature Publishing Group, 2016, doi:10.1038/srep36440.
short: J. Schwarz, V. Bierbaum, J. Merrin, T. Frank, R. Hauschild, M.T. Bollenbach,
S. Tay, M.K. Sixt, M. Mehling, Scientific Reports 6 (2016).
date_created: 2018-12-11T11:50:27Z
date_published: 2016-11-07T00:00:00Z
date_updated: 2021-01-12T06:48:41Z
day: '07'
ddc:
- '579'
department:
- _id: MiSi
- _id: NanoFab
- _id: Bio
- _id: ToBo
doi: 10.1038/srep36440
ec_funded: 1
file:
- access_level: open_access
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:32Z
date_updated: 2018-12-12T10:09:32Z
file_id: '4756'
file_name: IST-2017-744-v1+1_srep36440.pdf
file_size: 2353456
relation: main_file
file_date_updated: 2018-12-12T10:09:32Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Scientific Reports
publication_status: published
publisher: Nature Publishing Group
publist_id: '6204'
pubrep_id: '744'
quality_controlled: '1'
scopus_import: 1
status: public
title: A microfluidic device for measuring cell migration towards substrate bound
and soluble chemokine gradients
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2016'
...
---
_id: '1201'
abstract:
- lang: eng
text: In this issue of Cell, Skau et al. show that the formin FMN2 organizes a perinuclear
actin cytoskeleton that protects the nucleus and its genomic content of migrating
cells squeezing through small spaces.
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Renkawitz J, Sixt MK. Formin’ a nuclear protection. Cell. 2016;167(6):1448-1449.
doi:10.1016/j.cell.2016.11.024
apa: Renkawitz, J., & Sixt, M. K. (2016). Formin’ a nuclear protection. Cell.
Cell Press. https://doi.org/10.1016/j.cell.2016.11.024
chicago: Renkawitz, Jörg, and Michael K Sixt. “Formin’ a Nuclear Protection.” Cell.
Cell Press, 2016. https://doi.org/10.1016/j.cell.2016.11.024.
ieee: J. Renkawitz and M. K. Sixt, “Formin’ a nuclear protection,” Cell,
vol. 167, no. 6. Cell Press, pp. 1448–1449, 2016.
ista: Renkawitz J, Sixt MK. 2016. Formin’ a nuclear protection. Cell. 167(6), 1448–1449.
mla: Renkawitz, Jörg, and Michael K. Sixt. “Formin’ a Nuclear Protection.” Cell,
vol. 167, no. 6, Cell Press, 2016, pp. 1448–49, doi:10.1016/j.cell.2016.11.024.
short: J. Renkawitz, M.K. Sixt, Cell 167 (2016) 1448–1449.
date_created: 2018-12-11T11:50:41Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2021-01-12T06:49:03Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/j.cell.2016.11.024
intvolume: ' 167'
issue: '6'
language:
- iso: eng
month: '12'
oa_version: None
page: 1448 - 1449
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '6149'
quality_controlled: '1'
scopus_import: 1
status: public
title: Formin’ a nuclear protection
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 167
year: '2016'
...
---
_id: '1217'
abstract:
- lang: eng
text: Understanding the regulation of T-cell responses during inflammation and auto-immunity
is fundamental for designing efficient therapeutic strategies against immune diseases.
In this regard, prostaglandin E 2 (PGE 2) is mostly considered a myeloid-derived
immunosuppressive molecule. We describe for the first time that T cells secrete
PGE 2 during T-cell receptor stimulation. In addition, we show that autocrine
PGE 2 signaling through EP receptors is essential for optimal CD4 + T-cell activation
in vitro and in vivo, and for T helper 1 (Th1) and regulatory T cell differentiation.
PGE 2 was found to provide additive co-stimulatory signaling through AKT activation.
Intravital multiphoton microscopy showed that triggering EP receptors in T cells
is also essential for the stability of T cell-dendritic cell (DC) interactions
and Th-cell accumulation in draining lymph nodes (LNs) during inflammation. We
further demonstrated that blocking EP receptors in T cells during the initial
phase of collagen-induced arthritis in mice resulted in a reduction of clinical
arthritis. This could be attributable to defective T-cell activation, accompanied
by a decline in activated and interferon-γ-producing CD4 + Th1 cells in draining
LNs. In conclusion, we prove that T lymphocytes secret picomolar concentrations
of PGE 2, which in turn provide additive co-stimulatory signaling, enabling T
cells to attain a favorable activation threshold. PGE 2 signaling in T cells is
also required for maintaining long and stable interactions with DCs within LNs.
Blockade of EP receptors in vivo impairs T-cell activation and development of
T cell-mediated inflammatory responses. This may have implications in various
pathophysiological settings.
acknowledgement: This manuscript has been supported by grants SAF2007-61716 and S-SAL-0159/2006
awarded by the Spanish Ministry of Science and Education and the Community of Madrid
to Dr M Fresno.
author:
- first_name: Vinatha
full_name: Sreeramkumar, Vinatha
last_name: Sreeramkumar
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Carmen
full_name: Punzón, Carmen
last_name: Punzón
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: David
full_name: Sancho, David
last_name: Sancho
- first_name: Manuel
full_name: Fresno Forcelledo, Manuel
last_name: Fresno Forcelledo
- first_name: Natalia
full_name: Cuesta, Natalia
last_name: Cuesta
citation:
ama: Sreeramkumar V, Hons M, Punzón C, et al. Efficient T-cell priming and activation
requires signaling through prostaglandin E2 (EP) receptors. Immunology and
Cell Biology. 2016;94(1):39-51. doi:10.1038/icb.2015.62
apa: Sreeramkumar, V., Hons, M., Punzón, C., Stein, J., Sancho, D., Fresno Forcelledo,
M., & Cuesta, N. (2016). Efficient T-cell priming and activation requires
signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology.
Nature Publishing Group. https://doi.org/10.1038/icb.2015.62
chicago: Sreeramkumar, Vinatha, Miroslav Hons, Carmen Punzón, Jens Stein, David
Sancho, Manuel Fresno Forcelledo, and Natalia Cuesta. “Efficient T-Cell Priming
and Activation Requires Signaling through Prostaglandin E2 (EP) Receptors.” Immunology
and Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/icb.2015.62.
ieee: V. Sreeramkumar et al., “Efficient T-cell priming and activation requires
signaling through prostaglandin E2 (EP) receptors,” Immunology and Cell Biology,
vol. 94, no. 1. Nature Publishing Group, pp. 39–51, 2016.
ista: Sreeramkumar V, Hons M, Punzón C, Stein J, Sancho D, Fresno Forcelledo M,
Cuesta N. 2016. Efficient T-cell priming and activation requires signaling through
prostaglandin E2 (EP) receptors. Immunology and Cell Biology. 94(1), 39–51.
mla: Sreeramkumar, Vinatha, et al. “Efficient T-Cell Priming and Activation Requires
Signaling through Prostaglandin E2 (EP) Receptors.” Immunology and Cell Biology,
vol. 94, no. 1, Nature Publishing Group, 2016, pp. 39–51, doi:10.1038/icb.2015.62.
short: V. Sreeramkumar, M. Hons, C. Punzón, J. Stein, D. Sancho, M. Fresno Forcelledo,
N. Cuesta, Immunology and Cell Biology 94 (2016) 39–51.
date_created: 2018-12-11T11:50:46Z
date_published: 2016-01-01T00:00:00Z
date_updated: 2021-01-12T06:49:09Z
day: '01'
department:
- _id: MiSi
doi: 10.1038/icb.2015.62
intvolume: ' 94'
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 39 - 51
publication: Immunology and Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '6116'
quality_controlled: '1'
scopus_import: 1
status: public
title: Efficient T-cell priming and activation requires signaling through prostaglandin
E2 (EP) receptors
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 94
year: '2016'
...
---
_id: '1285'
abstract:
- lang: eng
text: Cell migration is central to a multitude of physiological processes, including
embryonic development, immune surveillance, and wound healing, and deregulated
migration is key to cancer dissemination. Decades of investigations have uncovered
many of the molecular and physical mechanisms underlying cell migration. Together
with protrusion extension and cell body retraction, adhesion to the substrate
via specific focal adhesion points has long been considered an essential step
in cell migration. Although this is true for cells moving on two-dimensional substrates,
recent studies have demonstrated that focal adhesions are not required for cells
moving in three dimensions, in which confinement is sufficient to maintain a cell
in contact with its substrate. Here, we review the investigations that have led
to challenging the requirement of specific adhesions for migration, discuss the
physical mechanisms proposed for cell body translocation during focal adhesion-independent
migration, and highlight the remaining open questions for the future.
acknowledgement: We would like to thank Dani Bodor for critical comments on the manuscript
and Guillaume Salbreux for discussions. The authors are supported by the United
Kingdom's Medical Research Council (MRC) (E.K.P. and I.M.A.; core funding to the
MRC Laboratory for Molecular Cell Biology), by the European Research Council [ERC
GA 311637 (E.K.P.) and ERC GA 281556 (M.S.)], and by a START award from the Austrian
Science Foundation (M.S.).
author:
- first_name: Ewa
full_name: Paluch, Ewa
last_name: Paluch
- first_name: Irene
full_name: Aspalter, Irene
last_name: Aspalter
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Paluch E, Aspalter I, Sixt MK. Focal adhesion-independent cell migration. Annual
Review of Cell and Developmental Biology. 2016;32:469-490. doi:10.1146/annurev-cellbio-111315-125341
apa: Paluch, E., Aspalter, I., & Sixt, M. K. (2016). Focal adhesion-independent
cell migration. Annual Review of Cell and Developmental Biology. Annual
Reviews. https://doi.org/10.1146/annurev-cellbio-111315-125341
chicago: Paluch, Ewa, Irene Aspalter, and Michael K Sixt. “Focal Adhesion-Independent
Cell Migration.” Annual Review of Cell and Developmental Biology. Annual
Reviews, 2016. https://doi.org/10.1146/annurev-cellbio-111315-125341.
ieee: E. Paluch, I. Aspalter, and M. K. Sixt, “Focal adhesion-independent cell migration,”
Annual Review of Cell and Developmental Biology, vol. 32. Annual Reviews,
pp. 469–490, 2016.
ista: Paluch E, Aspalter I, Sixt MK. 2016. Focal adhesion-independent cell migration.
Annual Review of Cell and Developmental Biology. 32, 469–490.
mla: Paluch, Ewa, et al. “Focal Adhesion-Independent Cell Migration.” Annual
Review of Cell and Developmental Biology, vol. 32, Annual Reviews, 2016, pp.
469–90, doi:10.1146/annurev-cellbio-111315-125341.
short: E. Paluch, I. Aspalter, M.K. Sixt, Annual Review of Cell and Developmental
Biology 32 (2016) 469–490.
date_created: 2018-12-11T11:51:08Z
date_published: 2016-10-06T00:00:00Z
date_updated: 2021-01-12T06:49:37Z
day: '06'
department:
- _id: MiSi
doi: 10.1146/annurev-cellbio-111315-125341
ec_funded: 1
intvolume: ' 32'
language:
- iso: eng
month: '10'
oa_version: None
page: 469 - 490
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Annual Review of Cell and Developmental Biology
publication_status: published
publisher: Annual Reviews
publist_id: '6031'
quality_controlled: '1'
scopus_import: 1
status: public
title: Focal adhesion-independent cell migration
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 32
year: '2016'
...
---
_id: '1490'
abstract:
- lang: eng
text: To induce adaptive immunity, dendritic cells (DCs) migrate through afferent
lymphatic vessels (LVs) to draining lymph nodes (dLNs). This process occurs in
several consecutive steps. Upon entry into lymphatic capillaries, DCs first actively
crawl into downstream collecting vessels. From there, they are next passively
and rapidly transported to the dLN by lymph flow. Here, we describe a role for
the chemokine CCL21 in intralymphatic DC crawling. Performing time-lapse imaging
in murine skin, we found that blockade of CCL21-but not the absence of lymph flow-completely
abolished DC migration from capillaries toward collecting vessels and reduced
the ability of intralymphatic DCs to emigrate from skin. Moreover, we found that
in vitro low laminar flow established a CCL21 gradient along lymphatic endothelial
monolayers, thereby inducing downstream-directed DC migration. These findings
reveal a role for intralymphatic CCL21 in promoting DC trafficking to dLNs, through
the formation of a flow-induced gradient.
author:
- first_name: Erica
full_name: Russo, Erica
last_name: Russo
- first_name: Alvaro
full_name: Teijeira, Alvaro
last_name: Teijeira
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Ann
full_name: Willrodt, Ann
last_name: Willrodt
- first_name: Joël
full_name: Bloch, Joël
last_name: Bloch
- first_name: Maximilian
full_name: Nitschké, Maximilian
last_name: Nitschké
- first_name: Laura
full_name: Santambrogio, Laura
last_name: Santambrogio
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Cornelia
full_name: Halin, Cornelia
last_name: Halin
citation:
ama: Russo E, Teijeira A, Vaahtomeri K, et al. Intralymphatic CCL21 promotes tissue
egress of dendritic cells through afferent lymphatic vessels. Cell Reports.
2016;14(7):1723-1734. doi:10.1016/j.celrep.2016.01.048
apa: Russo, E., Teijeira, A., Vaahtomeri, K., Willrodt, A., Bloch, J., Nitschké,
M., … Halin, C. (2016). Intralymphatic CCL21 promotes tissue egress of dendritic
cells through afferent lymphatic vessels. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2016.01.048
chicago: Russo, Erica, Alvaro Teijeira, Kari Vaahtomeri, Ann Willrodt, Joël Bloch,
Maximilian Nitschké, Laura Santambrogio, Dontscho Kerjaschki, Michael K Sixt,
and Cornelia Halin. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic
Cells through Afferent Lymphatic Vessels.” Cell Reports. Cell Press, 2016.
https://doi.org/10.1016/j.celrep.2016.01.048.
ieee: E. Russo et al., “Intralymphatic CCL21 promotes tissue egress of dendritic
cells through afferent lymphatic vessels,” Cell Reports, vol. 14, no. 7.
Cell Press, pp. 1723–1734, 2016.
ista: Russo E, Teijeira A, Vaahtomeri K, Willrodt A, Bloch J, Nitschké M, Santambrogio
L, Kerjaschki D, Sixt MK, Halin C. 2016. Intralymphatic CCL21 promotes tissue
egress of dendritic cells through afferent lymphatic vessels. Cell Reports. 14(7),
1723–1734.
mla: Russo, Erica, et al. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic
Cells through Afferent Lymphatic Vessels.” Cell Reports, vol. 14, no. 7,
Cell Press, 2016, pp. 1723–34, doi:10.1016/j.celrep.2016.01.048.
short: E. Russo, A. Teijeira, K. Vaahtomeri, A. Willrodt, J. Bloch, M. Nitschké,
L. Santambrogio, D. Kerjaschki, M.K. Sixt, C. Halin, Cell Reports 14 (2016) 1723–1734.
date_created: 2018-12-11T11:52:19Z
date_published: 2016-02-23T00:00:00Z
date_updated: 2021-01-12T06:51:07Z
day: '23'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.celrep.2016.01.048
file:
- access_level: open_access
checksum: c98c1151d5f1e5ce1643a83d8d7f3c29
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:12:30Z
date_updated: 2020-07-14T12:44:58Z
file_id: '4948'
file_name: IST-2016-515-v1+1_1-s2.0-S2211124716300262-main.pdf
file_size: 5489897
relation: main_file
file_date_updated: 2020-07-14T12:44:58Z
has_accepted_license: '1'
intvolume: ' 14'
issue: '7'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '02'
oa: 1
oa_version: Published Version
page: 1723 - 1734
publication: Cell Reports
publication_status: published
publisher: Cell Press
publist_id: '5697'
pubrep_id: '515'
quality_controlled: '1'
scopus_import: 1
status: public
title: Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent
lymphatic vessels
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 14
year: '2016'
...
---
_id: '1599'
abstract:
- lang: eng
text: "The addition of polysialic acid to N- and/or O-linked glycans, referred to
as polysialylation, is a rare posttranslational modification that is mainly known
to control the developmental plasticity of the nervous system. Here we show that
CCR7, the central chemokine receptor controlling immune cell trafficking to secondary
lymphatic organs, carries polysialic acid. This modification is essential for
the recognition of the CCR7 ligand CCL21. As a consequence, dendritic cell trafficking
is abrogated in polysialyltransferase-deficient mice, manifesting as disturbed
lymph node homeostasis and unresponsiveness to inflammatory stimuli. Structure-function
analysis of chemokine-receptor interactions reveals that CCL21 adopts an autoinhibited
conformation, which is released upon interaction with polysialic acid. Thus, we
describe a glycosylation-mediated immune cell trafficking disorder and its mechanistic
basis.\r\n"
acknowledged_ssus:
- _id: SSU
acknowledgement: 'We thank S. Schüchner and E. Ogris for kindly providing the antibody
to GFP, M. Helmbrecht and A. Huber for providing Nrp2−/− mice, the IST Scientific
Support Facilities for excellent services, and J. Renkawitz and K. Vaahtomeri for
critically reading the manuscript. '
article_processing_charge: No
article_type: original
author:
- first_name: Eva
full_name: Kiermaier, Eva
id: 3EB04B78-F248-11E8-B48F-1D18A9856A87
last_name: Kiermaier
orcid: 0000-0001-6165-5738
- first_name: Christine
full_name: Moussion, Christine
id: 3356F664-F248-11E8-B48F-1D18A9856A87
last_name: Moussion
- first_name: Christopher
full_name: Veldkamp, Christopher
last_name: Veldkamp
- first_name: Rita
full_name: Gerardy Schahn, Rita
last_name: Gerardy Schahn
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Larry
full_name: Williams, Larry
last_name: Williams
- first_name: Gary
full_name: Chaffee, Gary
last_name: Chaffee
- first_name: Andrew
full_name: Phillips, Andrew
last_name: Phillips
- first_name: Friedrich
full_name: Freiberger, Friedrich
last_name: Freiberger
- first_name: Richard
full_name: Imre, Richard
last_name: Imre
- first_name: Deni
full_name: Taleski, Deni
last_name: Taleski
- first_name: Richard
full_name: Payne, Richard
last_name: Payne
- first_name: Asolina
full_name: Braun, Asolina
last_name: Braun
- first_name: Reinhold
full_name: Förster, Reinhold
last_name: Förster
- first_name: Karl
full_name: Mechtler, Karl
last_name: Mechtler
- first_name: Martina
full_name: Mühlenhoff, Martina
last_name: Mühlenhoff
- first_name: Brian
full_name: Volkman, Brian
last_name: Volkman
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Kiermaier E, Moussion C, Veldkamp C, et al. Polysialylation controls dendritic
cell trafficking by regulating chemokine recognition. Science. 2016;351(6269):186-190.
doi:10.1126/science.aad0512
apa: Kiermaier, E., Moussion, C., Veldkamp, C., Gerardy Schahn, R., de Vries, I.,
Williams, L., … Sixt, M. K. (2016). Polysialylation controls dendritic cell trafficking
by regulating chemokine recognition. Science. American Association for
the Advancement of Science. https://doi.org/10.1126/science.aad0512
chicago: Kiermaier, Eva, Christine Moussion, Christopher Veldkamp, Rita Gerardy
Schahn, Ingrid de Vries, Larry Williams, Gary Chaffee, et al. “Polysialylation
Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” Science.
American Association for the Advancement of Science, 2016. https://doi.org/10.1126/science.aad0512.
ieee: E. Kiermaier et al., “Polysialylation controls dendritic cell trafficking
by regulating chemokine recognition,” Science, vol. 351, no. 6269. American
Association for the Advancement of Science, pp. 186–190, 2016.
ista: Kiermaier E, Moussion C, Veldkamp C, Gerardy Schahn R, de Vries I, Williams
L, Chaffee G, Phillips A, Freiberger F, Imre R, Taleski D, Payne R, Braun A, Förster
R, Mechtler K, Mühlenhoff M, Volkman B, Sixt MK. 2016. Polysialylation controls
dendritic cell trafficking by regulating chemokine recognition. Science. 351(6269),
186–190.
mla: Kiermaier, Eva, et al. “Polysialylation Controls Dendritic Cell Trafficking
by Regulating Chemokine Recognition.” Science, vol. 351, no. 6269, American
Association for the Advancement of Science, 2016, pp. 186–90, doi:10.1126/science.aad0512.
short: E. Kiermaier, C. Moussion, C. Veldkamp, R. Gerardy Schahn, I. de Vries,
L. Williams, G. Chaffee, A. Phillips, F. Freiberger, R. Imre, D. Taleski, R. Payne,
A. Braun, R. Förster, K. Mechtler, M. Mühlenhoff, B. Volkman, M.K. Sixt, Science
351 (2016) 186–190.
date_created: 2018-12-11T11:52:57Z
date_published: 2016-01-08T00:00:00Z
date_updated: 2021-01-12T06:51:52Z
day: '08'
department:
- _id: MiSi
doi: 10.1126/science.aad0512
ec_funded: 1
external_id:
pmid:
- '26657283'
intvolume: ' 351'
issue: '6269'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583642/
month: '01'
oa: 1
oa_version: Submitted Version
page: 186 - 190
pmid: 1
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A76F58-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '289720'
name: Stromal Cell-immune Cell Interactions in Health and Disease
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5570'
quality_controlled: '1'
scopus_import: 1
status: public
title: Polysialylation controls dendritic cell trafficking by regulating chemokine
recognition
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 351
year: '2016'
...
---
_id: '1597'
abstract:
- lang: eng
text: Chemokines are the main guidance cues directing leukocyte migration. Opposed
to early assumptions, chemokines do not necessarily act as soluble cues but are
often immobilized within tissues, e.g., dendritic cell migration toward lymphatic
vessels is guided by a haptotactic gradient of the chemokine CCL21. Controlled
assay systems to quantitatively study haptotaxis in vitro are still missing. In
this chapter, we describe an in vitro haptotaxis assay optimized for the unique
properties of dendritic cells. The chemokine CCL21 is immobilized in a bioactive
state, using laser-assisted protein adsorption by photobleaching. The cells follow
this immobilized CCL21 gradient in a haptotaxis chamber, which provides three
dimensionally confined migration conditions.
acknowledged_ssus:
- _id: Bio
acknowledgement: This work was supported by the Boehringer Ingelheim Fonds, the European
Research Council (ERC StG 281556), and a START Award of the Austrian Science Foundation
(FWF). We thank Robert Hauschild, Anne Reversat, and Jack Merrin for valuable input
and the Imaging Facility of IST Austria for excellent support.
article_processing_charge: No
article_type: original
author:
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Schwarz J, Sixt MK. Quantitative analysis of dendritic cell haptotaxis. Methods
in Enzymology. 2016;570:567-581. doi:10.1016/bs.mie.2015.11.004
apa: Schwarz, J., & Sixt, M. K. (2016). Quantitative analysis of dendritic cell
haptotaxis. Methods in Enzymology. Elsevier. https://doi.org/10.1016/bs.mie.2015.11.004
chicago: Schwarz, Jan, and Michael K Sixt. “Quantitative Analysis of Dendritic Cell
Haptotaxis.” Methods in Enzymology. Elsevier, 2016. https://doi.org/10.1016/bs.mie.2015.11.004.
ieee: J. Schwarz and M. K. Sixt, “Quantitative analysis of dendritic cell haptotaxis,”
Methods in Enzymology, vol. 570. Elsevier, pp. 567–581, 2016.
ista: Schwarz J, Sixt MK. 2016. Quantitative analysis of dendritic cell haptotaxis.
Methods in Enzymology. 570, 567–581.
mla: Schwarz, Jan, and Michael K. Sixt. “Quantitative Analysis of Dendritic Cell
Haptotaxis.” Methods in Enzymology, vol. 570, Elsevier, 2016, pp. 567–81,
doi:10.1016/bs.mie.2015.11.004.
short: J. Schwarz, M.K. Sixt, Methods in Enzymology 570 (2016) 567–581.
date_created: 2018-12-11T11:52:56Z
date_published: 2016-01-01T00:00:00Z
date_updated: 2021-01-12T06:51:51Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/bs.mie.2015.11.004
ec_funded: 1
external_id:
pmid:
- '26921962'
intvolume: ' 570'
language:
- iso: eng
month: '01'
oa_version: None
page: 567 - 581
pmid: 1
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Methods in Enzymology
publication_status: published
publisher: Elsevier
publist_id: '5573'
quality_controlled: '1'
scopus_import: 1
status: public
title: Quantitative analysis of dendritic cell haptotaxis
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 570
year: '2016'
...
---
_id: '1129'
abstract:
- lang: eng
text: "Directed cell migration is a hallmark feature, present in almost all multi-cellular\r\norganisms.
Despite its importance, basic questions regarding force transduction\r\nor directional
sensing are still heavily investigated. Directed migration of cells\r\nguided
by immobilized guidance cues - haptotaxis - occurs in key-processes,\r\nsuch as
embryonic development and immunity (Middleton et al., 1997; Nguyen\r\net al.,
2000; Thiery, 1984; Weber et al., 2013). Immobilized guidance cues\r\ncomprise
adhesive ligands, such as collagen and fibronectin (Barczyk et al.,\r\n2009),
or chemokines - the main guidance cues for migratory leukocytes\r\n(Middleton
et al., 1997; Weber et al., 2013). While adhesive ligands serve as\r\nattachment
sites guiding cell migration (Carter, 1965), chemokines instruct\r\nhaptotactic
migration by inducing adhesion to adhesive ligands and directional\r\nguidance
(Rot and Andrian, 2004; Schumann et al., 2010). Quantitative analysis\r\nof the
cellular response to immobilized guidance cues requires in vitro assays\r\nthat
foster cell migration, offer accurate control of the immobilized cues on a\r\nsubcellular
scale and in the ideal case closely reproduce in vivo conditions. The\r\nexploration
of haptotactic cell migration through design and employment of such\r\nassays
represents the main focus of this work.\r\nDendritic cells (DCs) are leukocytes,
which after encountering danger\r\nsignals such as pathogens in peripheral organs
instruct naïve T-cells and\r\nconsequently the adaptive immune response in the
lymph node (Mellman and\r\nSteinman, 2001). To reach the lymph node from the periphery,
DCs follow\r\nhaptotactic gradients of the chemokine CCL21 towards lymphatic vessels\r\n(Weber
et al., 2013). Questions about how DCs interpret haptotactic CCL21\r\ngradients
have not yet been addressed. The main reason for this is the lack of\r\nan assay
that offers diverse haptotactic environments, hence allowing the study\r\nof DC
migration as a response to different signals of immobilized guidance cue.\r\nIn
this work, we developed an in vitro assay that enables us to\r\nquantitatively
assess DC haptotaxis, by combining precisely controllable\r\nchemokine photo-patterning
with physically confining migration conditions. With this tool at hand, we studied
the influence of CCL21 gradient properties and\r\nconcentration on DC haptotaxis.
We found that haptotactic gradient sensing\r\ndepends on the absolute CCL21 concentration
in combination with the local\r\nsteepness of the gradient. Our analysis suggests
that the directionality of\r\nmigrating DCs is governed by the signal-to-noise
ratio of CCL21 binding to its\r\nreceptor CCR7. Moreover, the haptotactic CCL21
gradient formed in vivo\r\nprovides an optimal shape for DCs to recognize haptotactic
guidance cue.\r\nBy reconstitution of the CCL21 gradient in vitro we were also
able to\r\nstudy the influence of CCR7 signal termination on DC haptotaxis. To
this end,\r\nwe used DCs lacking the G-protein coupled receptor kinase GRK6, which
is\r\nresponsible for CCL21 induced CCR7 receptor phosphorylation and\r\ndesensitization
(Zidar et al., 2009). We found that CCR7 desensitization by\r\nGRK6 is crucial
for maintenance of haptotactic CCL21 gradient sensing in vitro\r\nand confirm
those observations in vivo.\r\nIn the context of the organism, immobilized haptotactic
guidance cues\r\noften coincide and compete with soluble chemotactic guidance
cues. During\r\nwound healing, fibroblasts are exposed and influenced by adhesive
cues and\r\nsoluble factors at the same time (Wu et al., 2012; Wynn, 2008). Similarly,\r\nmigrating
DCs are exposed to both, soluble chemokines (CCL19 and truncated\r\nCCL21) inducing
chemotactic behavior as well as the immobilized CCL21. To\r\nquantitatively assess
these complex coinciding immobilized and soluble\r\nguidance cues, we implemented
our chemokine photo-patterning technique in a\r\nmicrofluidic system allowing
for chemotactic gradient generation. To validate\r\nthe assay, we observed DC
migration in competing CCL19/CCL21\r\nenvironments.\r\nAdhesiveness guided haptotaxis
has been studied intensively over the\r\nlast century. However, quantitative studies
leading to conceptual models are\r\nlargely missing, again due to the lack of
a precisely controllable in vitro assay. A\r\nrequirement for such an in vitro
assay is that it must prevent any uncontrolled\r\ncell adhesion. This can be accomplished
by stable passivation of the surface. In\r\naddition, controlled adhesion must
be sustainable, quantifiable and dose\r\ndependent in order to create homogenous
gradients. Therefore, we developed a novel covalent photo-patterning technique
satisfying all these needs. In\r\ncombination with a sustainable poly-vinyl alcohol
(PVA) surface coating we\r\nwere able to generate gradients of adhesive cue to
direct cell migration. This\r\napproach allowed us to characterize the haptotactic
migratory behavior of\r\nzebrafish keratocytes in vitro. Furthermore, defined
patterns of adhesive cue\r\nallowed us to control for cell shape and growth on
a subcellular scale."
acknowledged_ssus:
- _id: Bio
- _id: PreCl
- _id: LifeSc
acknowledgement: "First, I would like to thank Michael Sixt for being a great supervisor,
mentor and\r\nscientist. I highly appreciate his guidance and continued support.
Furthermore, I\r\nam very grateful that he gave me the exceptional opportunity to
pursue many\r\nideas of which some managed to be included in this thesis.\r\nI owe
sincere thanks to the members of my PhD thesis committee, Daria\r\nSiekhaus, Daniel
Legler and Harald Janovjak. Especially I would like to thank\r\nDaria for her advice
and encouragement during our regular progress meetings.\r\nI also want to thank
the team and fellows of the Boehringer Ingelheim Fond\r\n(BIF) PhD Fellowship for
amazing and inspiring meetings and the BIF for\r\nfinancial support.\r\nImportant
factors for the success of this thesis were the warm, creative\r\nand helpful atmosphere
as well as the team spirit of the whole Sixt Lab.\r\nTherefore I would like to thank
my current and former colleagues Frank Assen,\r\nMarkus Brown, Ingrid de Vries,
Michelle Duggan, Alexander Eichner, Miroslav\r\nHons, Eva Kiermaier, Aglaja Kopf,
Alexander Leithner, Christine Moussion, Jan\r\nMüller, Maria Nemethova, Jörg Renkawitz,
Anne Reversat, Kari Vaahtomeri,\r\nMichele Weber and Stefan Wieser. We had an amazing
time with many\r\nlegendary evenings and events. Along these lines I want to thank
the in vitro\r\ncrew of the lab, Jörg, Anne and Alex, for lots of ideas and productive\r\ndiscussions.
I am sure, some day we will reveal the secret of the ‘splodge’.\r\nI want to thank
the members of the Heisenberg Lab for a great time and\r\nthrilling kicker matches.
In this regard I especially want to thank Maurizio\r\n‘Gnocci’ Monti, Gabriel Krens,
Alex Eichner, Martin Behrndt, Vanessa Barone,Philipp Schmalhorst, Michael Smutny,
Daniel Capek, Anne Reversat, Eva\r\nKiermaier, Frank Assen and Jan Müller for wonderful
after-lunch matches.\r\nI would not have been able to analyze the thousands of cell
trajectories\r\nand probably hundreds of thousands of mouse clicks without the productive\r\ncollaboration
with Veronika Bierbaum and Tobias Bollenbach. Thanks Vroni for\r\ncountless meetings,
discussions and graphs and of course for proofreading and\r\nadvice for this thesis.
For proofreading I also want to thank Evi, Jörg, Jack and\r\nAnne.\r\nI would like
to acknowledge Matthias Mehling for a very productive\r\ncollaboration and for introducing
me into the wild world of microfluidics. Jack\r\nMerrin, for countless wafers, PDMS
coated coverslips and help with anything\r\nmicro-fabrication related. And Maria
Nemethova for establishing the ‘click’\r\npatterning approach with me. Without her
it still would be just one of the ideas…\r\nMany thanks to Ekaterina Papusheva,
Robert Hauschild, Doreen Milius\r\nand Nasser Darwish from the Bioimaging Facility
as well as the Preclinical and\r\nthe Life Science facilities of IST Austria for
excellent technical support. At this\r\npoint I especially want to thank Robert
for countless image analyses and\r\ntechnical ideas. Always interested and creative
he played an essential role in all\r\nof my projects.\r\nAdditionally I want to
thank Ingrid and Gabby for welcoming me warmly\r\nwhen I first started at IST, for
scientific and especially mental support in all\r\nthose years, countless coffee
sessions and Heurigen evenings. #BioimagingFacility #LifeScienceFacility #PreClinicalFacility"
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
citation:
ama: Schwarz J. Quantitative analysis of haptotactic cell migration. 2016.
apa: Schwarz, J. (2016). Quantitative analysis of haptotactic cell migration.
Institute of Science and Technology Austria.
chicago: Schwarz, Jan. “Quantitative Analysis of Haptotactic Cell Migration.” Institute
of Science and Technology Austria, 2016.
ieee: J. Schwarz, “Quantitative analysis of haptotactic cell migration,” Institute
of Science and Technology Austria, 2016.
ista: Schwarz J. 2016. Quantitative analysis of haptotactic cell migration. Institute
of Science and Technology Austria.
mla: Schwarz, Jan. Quantitative Analysis of Haptotactic Cell Migration. Institute
of Science and Technology Austria, 2016.
short: J. Schwarz, Quantitative Analysis of Haptotactic Cell Migration, Institute
of Science and Technology Austria, 2016.
date_created: 2018-12-11T11:50:18Z
date_published: 2016-07-01T00:00:00Z
date_updated: 2023-09-07T11:54:33Z
day: '01'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: MiSi
file:
- access_level: closed
checksum: e3cd6b28f9c5cccb8891855565a2dade
content_type: application/pdf
creator: dernst
date_created: 2019-08-13T10:55:35Z
date_updated: 2019-08-13T10:55:35Z
file_id: '6813'
file_name: Thesis_JSchwarz_final.pdf
file_size: 32044069
relation: main_file
- access_level: open_access
checksum: c3dbe219acf87eed2f46d21d5cca00de
content_type: application/pdf
creator: dernst
date_created: 2021-02-22T11:43:14Z
date_updated: 2021-02-22T11:43:14Z
file_id: '9181'
file_name: 2016_Thesis_JSchwarz.pdf
file_size: 8396717
relation: main_file
success: 1
file_date_updated: 2021-02-22T11:43:14Z
has_accepted_license: '1'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: '178'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '6231'
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: Quantitative analysis of haptotactic cell migration
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2016'
...
---
_id: '1321'
abstract:
- lang: eng
text: Most migrating cells extrude their front by the force of actin polymerization.
Polymerization requires an initial nucleation step, which is mediated by factors
establishing either parallel filaments in the case of filopodia or branched filaments
that form the branched lamellipodial network. Branches are considered essential
for regular cell motility and are initiated by the Arp2/3 complex, which in turn
is activated by nucleation-promoting factors of the WASP and WAVE families. Here
we employed rapid amoeboid crawling leukocytes and found that deletion of the
WAVE complex eliminated actin branching and thus lamellipodia formation. The cells
were left with parallel filaments at the leading edge, which translated, depending
on the differentiation status of the cell, into a unipolar pointed cell shape
or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased
speed and enormous directional persistence, while they were unable to turn towards
chemotactic gradients. Cells with multiple filopodia retained chemotactic activity
but their migration was progressively impaired with increasing geometrical complexity
of the extracellular environment. These findings establish that diversified leading
edge protrusions serve as explorative structures while they slow down actual locomotion.
acknowledged_ssus:
- _id: SSU
acknowledgement: "This work was supported by the German Research Foundation (DFG)
Priority Program SP 1464 to T.E.B.S. and M.S., and European Research Council (ERC
GA 281556) and Human Frontiers Program grants to M.S.\r\nService Units of IST Austria
for excellent technical support."
article_processing_charge: No
article_type: original
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: David
full_name: De Gorter, David
last_name: De Gorter
- first_name: Florian
full_name: Schur, Florian
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
- first_name: Jonathan
full_name: Bayerl, Jonathan
last_name: Bayerl
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Stefan
full_name: Wieser, Stefan
id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
last_name: Wieser
orcid: 0000-0002-2670-2217
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Frank
full_name: Lai, Frank
last_name: Lai
- first_name: Markus
full_name: Moser, Markus
last_name: Moser
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Victor
full_name: Small, Victor
last_name: Small
- first_name: Theresia
full_name: Stradal, Theresia
last_name: Stradal
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Leithner AF, Eichner A, Müller J, et al. Diversified actin protrusions promote
environmental exploration but are dispensable for locomotion of leukocytes. Nature
Cell Biology. 2016;18:1253-1259. doi:10.1038/ncb3426
apa: Leithner, A. F., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz,
J., … Sixt, M. K. (2016). Diversified actin protrusions promote environmental
exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology.
Nature Publishing Group. https://doi.org/10.1038/ncb3426
chicago: Leithner, Alexander F, Alexander Eichner, Jan Müller, Anne Reversat, Markus
Brown, Jan Schwarz, Jack Merrin, et al. “Diversified Actin Protrusions Promote
Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature
Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/ncb3426.
ieee: A. F. Leithner et al., “Diversified actin protrusions promote environmental
exploration but are dispensable for locomotion of leukocytes,” Nature Cell
Biology, vol. 18. Nature Publishing Group, pp. 1253–1259, 2016.
ista: Leithner AF, Eichner A, Müller J, Reversat A, Brown M, Schwarz J, Merrin J,
De Gorter D, Schur FK, Bayerl J, de Vries I, Wieser S, Hauschild R, Lai F, Moser
M, Kerjaschki D, Rottner K, Small V, Stradal T, Sixt MK. 2016. Diversified actin
protrusions promote environmental exploration but are dispensable for locomotion
of leukocytes. Nature Cell Biology. 18, 1253–1259.
mla: Leithner, Alexander F., et al. “Diversified Actin Protrusions Promote Environmental
Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell
Biology, vol. 18, Nature Publishing Group, 2016, pp. 1253–59, doi:10.1038/ncb3426.
short: A.F. Leithner, A. Eichner, J. Müller, A. Reversat, M. Brown, J. Schwarz,
J. Merrin, D. De Gorter, F.K. Schur, J. Bayerl, I. de Vries, S. Wieser, R. Hauschild,
F. Lai, M. Moser, D. Kerjaschki, K. Rottner, V. Small, T. Stradal, M.K. Sixt,
Nature Cell Biology 18 (2016) 1253–1259.
date_created: 2018-12-11T11:51:21Z
date_published: 2016-10-24T00:00:00Z
date_updated: 2024-03-28T23:30:16Z
day: '24'
ddc:
- '570'
department:
- _id: MiSi
- _id: NanoFab
- _id: Bio
doi: 10.1038/ncb3426
ec_funded: 1
file:
- access_level: open_access
checksum: e1411cb7c99a2d9089c178a6abef25e7
content_type: application/pdf
creator: dernst
date_created: 2020-05-14T16:33:46Z
date_updated: 2020-07-14T12:44:43Z
file_id: '7844'
file_name: 2018_NatureCell_Leithner.pdf
file_size: 4433280
relation: main_file
file_date_updated: 2020-07-14T12:44:43Z
has_accepted_license: '1'
intvolume: ' 18'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
month: '10'
oa: 1
oa_version: Submitted Version
page: 1253 - 1259
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '5949'
quality_controlled: '1'
related_material:
record:
- id: '323'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Diversified actin protrusions promote environmental exploration but are dispensable
for locomotion of leukocytes
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 18
year: '2016'
...
---
_id: '1530'
abstract:
- lang: eng
text: In growing cells, protein synthesis and cell growth are typically not synchronous,
and, thus, protein concentrations vary over the cell division cycle. We have developed
a theoretical description of genetic regulatory systems in bacteria that explicitly
considers the cell division cycle to investigate its impact on gene expression.
We calculate the cell-to-cell variations arising from cells being at different
stages in the division cycle for unregulated genes and for basic regulatory mechanisms.
These variations contribute to the extrinsic noise observed in single-cell experiments,
and are most significant for proteins with short lifetimes. Negative autoregulation
buffers against variation of protein concentration over the division cycle, but
the effect is found to be relatively weak. Stronger buffering is achieved by an
increased protein lifetime. Positive autoregulation can strongly amplify such
variation if the parameters are set to values that lead to resonance-like behaviour.
For cooperative positive autoregulation, the concentration variation over the
division cycle diminishes the parameter region of bistability and modulates the
switching times between the two stable states. The same effects are seen for a
two-gene mutual-repression toggle switch. By contrast, an oscillatory circuit,
the repressilator, is only weakly affected by the division cycle.
article_number: '066003'
author:
- first_name: Veronika
full_name: Bierbaum, Veronika
id: 3FD04378-F248-11E8-B48F-1D18A9856A87
last_name: Bierbaum
- first_name: Stefan
full_name: Klumpp, Stefan
last_name: Klumpp
citation:
ama: Bierbaum V, Klumpp S. Impact of the cell division cycle on gene circuits. Physical
Biology. 2015;12(6). doi:10.1088/1478-3975/12/6/066003
apa: Bierbaum, V., & Klumpp, S. (2015). Impact of the cell division cycle on
gene circuits. Physical Biology. IOP Publishing Ltd. https://doi.org/10.1088/1478-3975/12/6/066003
chicago: Bierbaum, Veronika, and Stefan Klumpp. “Impact of the Cell Division Cycle
on Gene Circuits.” Physical Biology. IOP Publishing Ltd., 2015. https://doi.org/10.1088/1478-3975/12/6/066003.
ieee: V. Bierbaum and S. Klumpp, “Impact of the cell division cycle on gene circuits,”
Physical Biology, vol. 12, no. 6. IOP Publishing Ltd., 2015.
ista: Bierbaum V, Klumpp S. 2015. Impact of the cell division cycle on gene circuits.
Physical Biology. 12(6), 066003.
mla: Bierbaum, Veronika, and Stefan Klumpp. “Impact of the Cell Division Cycle on
Gene Circuits.” Physical Biology, vol. 12, no. 6, 066003, IOP Publishing
Ltd., 2015, doi:10.1088/1478-3975/12/6/066003.
short: V. Bierbaum, S. Klumpp, Physical Biology 12 (2015).
date_created: 2018-12-11T11:52:33Z
date_published: 2015-09-25T00:00:00Z
date_updated: 2021-01-12T06:51:25Z
day: '25'
department:
- _id: MiSi
doi: 10.1088/1478-3975/12/6/066003
intvolume: ' 12'
issue: '6'
language:
- iso: eng
month: '09'
oa_version: None
publication: Physical Biology
publication_status: published
publisher: IOP Publishing Ltd.
publist_id: '5641'
quality_controlled: '1'
scopus_import: 1
status: public
title: Impact of the cell division cycle on gene circuits
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2015'
...
---
_id: '1553'
abstract:
- lang: eng
text: Cell movement has essential functions in development, immunity, and cancer.
Various cell migration patterns have been reported, but no general rule has emerged
so far. Here, we show on the basis of experimental data in vitro and in vivo that
cell persistence, which quantifies the straightness of trajectories, is robustly
coupled to cell migration speed. We suggest that this universal coupling constitutes
a generic law of cell migration, which originates in the advection of polarity
cues by an actin cytoskeleton undergoing flows at the cellular scale. Our analysis
relies on a theoretical model that we validate by measuring the persistence of
cells upon modulation of actin flow speeds and upon optogenetic manipulation of
the binding of an actin regulator to actin filaments. Beyond the quantitative
prediction of the coupling, the model yields a generic phase diagram of cellular
trajectories, which recapitulates the full range of observed migration patterns.
author:
- first_name: Paolo
full_name: Maiuri, Paolo
last_name: Maiuri
- first_name: Jean
full_name: Rupprecht, Jean
last_name: Rupprecht
- first_name: Stefan
full_name: Wieser, Stefan
id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
last_name: Wieser
orcid: 0000-0002-2670-2217
- first_name: Verena
full_name: Ruprecht, Verena
id: 4D71A03A-F248-11E8-B48F-1D18A9856A87
last_name: Ruprecht
orcid: 0000-0003-4088-8633
- first_name: Olivier
full_name: Bénichou, Olivier
last_name: Bénichou
- first_name: Nicolas
full_name: Carpi, Nicolas
last_name: Carpi
- first_name: Mathieu
full_name: Coppey, Mathieu
last_name: Coppey
- first_name: Simon
full_name: De Beco, Simon
last_name: De Beco
- first_name: Nir
full_name: Gov, Nir
last_name: Gov
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Carolina
full_name: Lage Crespo, Carolina
last_name: Lage Crespo
- first_name: Franziska
full_name: Lautenschlaeger, Franziska
last_name: Lautenschlaeger
- first_name: Maël
full_name: Le Berre, Maël
last_name: Le Berre
- first_name: Ana
full_name: Lennon Duménil, Ana
last_name: Lennon Duménil
- first_name: Matthew
full_name: Raab, Matthew
last_name: Raab
- first_name: Hawa
full_name: Thiam, Hawa
last_name: Thiam
- first_name: Matthieu
full_name: Piel, Matthieu
last_name: Piel
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Raphaël
full_name: Voituriez, Raphaël
last_name: Voituriez
citation:
ama: Maiuri P, Rupprecht J, Wieser S, et al. Actin flows mediate a universal coupling
between cell speed and cell persistence. Cell. 2015;161(2):374-386. doi:10.1016/j.cell.2015.01.056
apa: Maiuri, P., Rupprecht, J., Wieser, S., Ruprecht, V., Bénichou, O., Carpi, N.,
… Voituriez, R. (2015). Actin flows mediate a universal coupling between cell
speed and cell persistence. Cell. Cell Press. https://doi.org/10.1016/j.cell.2015.01.056
chicago: Maiuri, Paolo, Jean Rupprecht, Stefan Wieser, Verena Ruprecht, Olivier
Bénichou, Nicolas Carpi, Mathieu Coppey, et al. “Actin Flows Mediate a Universal
Coupling between Cell Speed and Cell Persistence.” Cell. Cell Press, 2015.
https://doi.org/10.1016/j.cell.2015.01.056.
ieee: P. Maiuri et al., “Actin flows mediate a universal coupling between
cell speed and cell persistence,” Cell, vol. 161, no. 2. Cell Press, pp.
374–386, 2015.
ista: Maiuri P, Rupprecht J, Wieser S, Ruprecht V, Bénichou O, Carpi N, Coppey M,
De Beco S, Gov N, Heisenberg C-PJ, Lage Crespo C, Lautenschlaeger F, Le Berre
M, Lennon Duménil A, Raab M, Thiam H, Piel M, Sixt MK, Voituriez R. 2015. Actin
flows mediate a universal coupling between cell speed and cell persistence. Cell.
161(2), 374–386.
mla: Maiuri, Paolo, et al. “Actin Flows Mediate a Universal Coupling between Cell
Speed and Cell Persistence.” Cell, vol. 161, no. 2, Cell Press, 2015, pp.
374–86, doi:10.1016/j.cell.2015.01.056.
short: P. Maiuri, J. Rupprecht, S. Wieser, V. Ruprecht, O. Bénichou, N. Carpi, M.
Coppey, S. De Beco, N. Gov, C.-P.J. Heisenberg, C. Lage Crespo, F. Lautenschlaeger,
M. Le Berre, A. Lennon Duménil, M. Raab, H. Thiam, M. Piel, M.K. Sixt, R. Voituriez,
Cell 161 (2015) 374–386.
date_created: 2018-12-11T11:52:41Z
date_published: 2015-04-09T00:00:00Z
date_updated: 2021-01-12T06:51:33Z
day: '09'
department:
- _id: MiSi
- _id: CaHe
doi: 10.1016/j.cell.2015.01.056
ec_funded: 1
intvolume: ' 161'
issue: '2'
language:
- iso: eng
month: '04'
oa_version: None
page: 374 - 386
project:
- _id: 2529486C-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T 560-B17
name: Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25ABD200-B435-11E9-9278-68D0E5697425
grant_number: RGP0058/2011
name: 'Cell migration in complex environments: from in vivo experiments to theoretical
models'
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '5618'
quality_controlled: '1'
scopus_import: 1
status: public
title: Actin flows mediate a universal coupling between cell speed and cell persistence
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 161
year: '2015'
...
---
_id: '1561'
abstract:
- lang: eng
text: Replication-deficient recombinant adenoviruses are potent vectors for the
efficient transient expression of exogenous genes in resting immune cells. However,
most leukocytes are refractory to efficient adenoviral transduction as they lack
expression of the coxsackie/adenovirus receptor (CAR). To circumvent this obstacle,
we generated the R26/CAG-CARΔ1StopF (where R26 is ROSA26 and CAG is CMV early
enhancer/chicken β actin promoter) knock-in mouse line. This strain allows monitoring
of in situ Cre recombinase activity through expression of CARΔ1. Simultaneously,
CARΔ1 expression permits selective and highly efficient adenoviral transduction
of immune cell populations, such as mast cells or T cells, directly ex vivo in
bulk cultures without prior cell purification or activation. Furthermore, we show
that CARΔ1 expression dramatically improves adenoviral infection of in vitro differentiated
conventional and plasmacytoid dendritic cells (DCs), basophils, mast cells, as
well as Hoxb8-immortalized hematopoietic progenitor cells. This novel dual function
mouse strain will hence be a valuable tool to rapidly dissect the function of
specific genes in leukocyte physiology.
author:
- first_name: Klaus
full_name: Heger, Klaus
last_name: Heger
- first_name: Maike
full_name: Kober, Maike
last_name: Kober
- first_name: David
full_name: Rieß, David
last_name: Rieß
- first_name: Christoph
full_name: Drees, Christoph
last_name: Drees
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Arianna
full_name: Bertossi, Arianna
last_name: Bertossi
- first_name: Axel
full_name: Roers, Axel
last_name: Roers
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Marc
full_name: Schmidt Supprian, Marc
last_name: Schmidt Supprian
citation:
ama: Heger K, Kober M, Rieß D, et al. A novel Cre recombinase reporter mouse strain
facilitates selective and efficient infection of primary immune cells with adenoviral
vectors. European Journal of Immunology. 2015;45(6):1614-1620. doi:10.1002/eji.201545457
apa: Heger, K., Kober, M., Rieß, D., Drees, C., de Vries, I., Bertossi, A., … Schmidt
Supprian, M. (2015). A novel Cre recombinase reporter mouse strain facilitates
selective and efficient infection of primary immune cells with adenoviral vectors.
European Journal of Immunology. Wiley. https://doi.org/10.1002/eji.201545457
chicago: Heger, Klaus, Maike Kober, David Rieß, Christoph Drees, Ingrid de Vries,
Arianna Bertossi, Axel Roers, Michael K Sixt, and Marc Schmidt Supprian. “A Novel
Cre Recombinase Reporter Mouse Strain Facilitates Selective and Efficient Infection
of Primary Immune Cells with Adenoviral Vectors.” European Journal of Immunology.
Wiley, 2015. https://doi.org/10.1002/eji.201545457.
ieee: K. Heger et al., “A novel Cre recombinase reporter mouse strain facilitates
selective and efficient infection of primary immune cells with adenoviral vectors,”
European Journal of Immunology, vol. 45, no. 6. Wiley, pp. 1614–1620, 2015.
ista: Heger K, Kober M, Rieß D, Drees C, de Vries I, Bertossi A, Roers A, Sixt MK,
Schmidt Supprian M. 2015. A novel Cre recombinase reporter mouse strain facilitates
selective and efficient infection of primary immune cells with adenoviral vectors.
European Journal of Immunology. 45(6), 1614–1620.
mla: Heger, Klaus, et al. “A Novel Cre Recombinase Reporter Mouse Strain Facilitates
Selective and Efficient Infection of Primary Immune Cells with Adenoviral Vectors.”
European Journal of Immunology, vol. 45, no. 6, Wiley, 2015, pp. 1614–20,
doi:10.1002/eji.201545457.
short: K. Heger, M. Kober, D. Rieß, C. Drees, I. de Vries, A. Bertossi, A. Roers,
M.K. Sixt, M. Schmidt Supprian, European Journal of Immunology 45 (2015) 1614–1620.
date_created: 2018-12-11T11:52:44Z
date_published: 2015-06-01T00:00:00Z
date_updated: 2021-01-12T06:51:36Z
day: '01'
department:
- _id: MiSi
doi: 10.1002/eji.201545457
intvolume: ' 45'
issue: '6'
language:
- iso: eng
month: '06'
oa_version: None
page: 1614 - 1620
publication: European Journal of Immunology
publication_status: published
publisher: Wiley
publist_id: '5610'
quality_controlled: '1'
scopus_import: 1
status: public
title: A novel Cre recombinase reporter mouse strain facilitates selective and efficient
infection of primary immune cells with adenoviral vectors
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 45
year: '2015'
...
---
_id: '1560'
abstract:
- lang: eng
text: Stromal cells in the subcapsular sinus of the lymph node 'decide' which cells
and molecules are allowed access to the deeper parenchyma. The glycoprotein PLVAP
is a crucial component of this selector function.
author:
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Hons M, Sixt MK. The lymph node filter revealed. Nature Immunology.
2015;16(4):338-340. doi:10.1038/ni.3126
apa: Hons, M., & Sixt, M. K. (2015). The lymph node filter revealed. Nature
Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3126
chicago: Hons, Miroslav, and Michael K Sixt. “The Lymph Node Filter Revealed.” Nature
Immunology. Nature Publishing Group, 2015. https://doi.org/10.1038/ni.3126.
ieee: M. Hons and M. K. Sixt, “The lymph node filter revealed,” Nature Immunology,
vol. 16, no. 4. Nature Publishing Group, pp. 338–340, 2015.
ista: Hons M, Sixt MK. 2015. The lymph node filter revealed. Nature Immunology.
16(4), 338–340.
mla: Hons, Miroslav, and Michael K. Sixt. “The Lymph Node Filter Revealed.” Nature
Immunology, vol. 16, no. 4, Nature Publishing Group, 2015, pp. 338–40, doi:10.1038/ni.3126.
short: M. Hons, M.K. Sixt, Nature Immunology 16 (2015) 338–340.
date_created: 2018-12-11T11:52:43Z
date_published: 2015-03-19T00:00:00Z
date_updated: 2021-01-12T06:51:36Z
day: '19'
department:
- _id: MiSi
doi: 10.1038/ni.3126
intvolume: ' 16'
issue: '4'
language:
- iso: eng
month: '03'
oa_version: None
page: 338 - 340
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '5611'
quality_controlled: '1'
scopus_import: 1
status: public
title: The lymph node filter revealed
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2015'
...
---
_id: '1575'
abstract:
- lang: eng
text: The immune response relies on the migration of leukocytes and on their ability
to stop in precise anatomical locations to fulfil their task. How leukocyte migration
and function are coordinated is unknown. Here we show that in immature dendritic
cells, which patrol their environment by engulfing extracellular material, cell
migration and antigen capture are antagonistic. This antagonism results from transient
enrichment of myosin IIA at the cell front, which disrupts the back-to-front gradient
of the motor protein, slowing down locomotion but promoting antigen capture. We
further highlight that myosin IIA enrichment at the cell front requires the MHC
class II-associated invariant chain (Ii). Thus, by controlling myosin IIA localization,
Ii imposes on dendritic cells an intermittent antigen capture behaviour that might
facilitate environment patrolling. We propose that the requirement for myosin
II in both cell migration and specific cell functions may provide a general mechanism
for their coordination in time and space.
acknowledgement: M.C. and M.L.H. were supported by fellowships from the Fondation
pour la Recherche Médicale and the Association pour la Recherche contre le Cancer,
respectively. This work was funded by grants from the City of Paris and the European
Research Council to A.-M.L.-D. (Strapacemi 243103), the Association Nationale pour
la Recherche (ANR-09-PIRI-0027-PCVI) and the InnaBiosanté foundation (Micemico)
to A.-M.L.-D., M.P. and R.V., and the DCBIOL Labex from the French Government (ANR-10-IDEX-0001-02-PSL*
and ANR-11-LABX-0043). The super-resolution SIM microscope was funded through an
ERC Advanced Investigator Grant (250367) to Edith Heard (CNRS UMR3215/Inserm U934,
Institut Curie).
article_number: '7526'
author:
- first_name: Mélanie
full_name: Chabaud, Mélanie
last_name: Chabaud
- first_name: Mélina
full_name: Heuzé, Mélina
last_name: Heuzé
- first_name: Marine
full_name: Bretou, Marine
last_name: Bretou
- first_name: Pablo
full_name: Vargas, Pablo
last_name: Vargas
- first_name: Paolo
full_name: Maiuri, Paolo
last_name: Maiuri
- first_name: Paola
full_name: Solanes, Paola
last_name: Solanes
- first_name: Mathieu
full_name: Maurin, Mathieu
last_name: Maurin
- first_name: Emmanuel
full_name: Terriac, Emmanuel
last_name: Terriac
- first_name: Maël
full_name: Le Berre, Maël
last_name: Le Berre
- first_name: Danielle
full_name: Lankar, Danielle
last_name: Lankar
- first_name: Tristan
full_name: Piolot, Tristan
last_name: Piolot
- first_name: Robert
full_name: Adelstein, Robert
last_name: Adelstein
- first_name: Yingfan
full_name: Zhang, Yingfan
last_name: Zhang
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Jordan
full_name: Jacobelli, Jordan
last_name: Jacobelli
- first_name: Olivier
full_name: Bénichou, Olivier
last_name: Bénichou
- first_name: Raphaël
full_name: Voituriez, Raphaël
last_name: Voituriez
- first_name: Matthieu
full_name: Piel, Matthieu
last_name: Piel
- first_name: Ana
full_name: Lennon Duménil, Ana
last_name: Lennon Duménil
citation:
ama: Chabaud M, Heuzé M, Bretou M, et al. Cell migration and antigen capture are
antagonistic processes coupled by myosin II in dendritic cells. Nature Communications.
2015;6. doi:10.1038/ncomms8526
apa: Chabaud, M., Heuzé, M., Bretou, M., Vargas, P., Maiuri, P., Solanes, P., …
Lennon Duménil, A. (2015). Cell migration and antigen capture are antagonistic
processes coupled by myosin II in dendritic cells. Nature Communications.
Nature Publishing Group. https://doi.org/10.1038/ncomms8526
chicago: Chabaud, Mélanie, Mélina Heuzé, Marine Bretou, Pablo Vargas, Paolo Maiuri,
Paola Solanes, Mathieu Maurin, et al. “Cell Migration and Antigen Capture Are
Antagonistic Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications.
Nature Publishing Group, 2015. https://doi.org/10.1038/ncomms8526.
ieee: M. Chabaud et al., “Cell migration and antigen capture are antagonistic
processes coupled by myosin II in dendritic cells,” Nature Communications,
vol. 6. Nature Publishing Group, 2015.
ista: Chabaud M, Heuzé M, Bretou M, Vargas P, Maiuri P, Solanes P, Maurin M, Terriac
E, Le Berre M, Lankar D, Piolot T, Adelstein R, Zhang Y, Sixt MK, Jacobelli J,
Bénichou O, Voituriez R, Piel M, Lennon Duménil A. 2015. Cell migration and antigen
capture are antagonistic processes coupled by myosin II in dendritic cells. Nature
Communications. 6, 7526.
mla: Chabaud, Mélanie, et al. “Cell Migration and Antigen Capture Are Antagonistic
Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications,
vol. 6, 7526, Nature Publishing Group, 2015, doi:10.1038/ncomms8526.
short: M. Chabaud, M. Heuzé, M. Bretou, P. Vargas, P. Maiuri, P. Solanes, M. Maurin,
E. Terriac, M. Le Berre, D. Lankar, T. Piolot, R. Adelstein, Y. Zhang, M.K. Sixt,
J. Jacobelli, O. Bénichou, R. Voituriez, M. Piel, A. Lennon Duménil, Nature Communications
6 (2015).
date_created: 2018-12-11T11:52:48Z
date_published: 2015-06-25T00:00:00Z
date_updated: 2021-01-12T06:51:42Z
day: '25'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1038/ncomms8526
file:
- access_level: open_access
checksum: bae12e86be2adb28253f890b8bba8315
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:58Z
date_updated: 2020-07-14T12:45:02Z
file_id: '4915'
file_name: IST-2016-476-v1+1_ncomms8526.pdf
file_size: 4530215
relation: main_file
file_date_updated: 2020-07-14T12:45:02Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_status: published
publisher: Nature Publishing Group
publist_id: '5596'
pubrep_id: '476'
quality_controlled: '1'
scopus_import: 1
status: public
title: Cell migration and antigen capture are antagonistic processes coupled by myosin
II in dendritic cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2015'
...
---
_id: '1676'
author:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Erez
full_name: Raz, Erez
last_name: Raz
citation:
ama: 'Sixt MK, Raz E. Editorial overview: Cell adhesion and migration. Current
Opinion in Cell Biology. 2015;36(10):4-6. doi:10.1016/j.ceb.2015.09.004'
apa: 'Sixt, M. K., & Raz, E. (2015). Editorial overview: Cell adhesion and migration.
Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.09.004'
chicago: 'Sixt, Michael K, and Erez Raz. “Editorial Overview: Cell Adhesion and
Migration.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.09.004.'
ieee: 'M. K. Sixt and E. Raz, “Editorial overview: Cell adhesion and migration,”
Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 4–6, 2015.'
ista: 'Sixt MK, Raz E. 2015. Editorial overview: Cell adhesion and migration. Current
Opinion in Cell Biology. 36(10), 4–6.'
mla: 'Sixt, Michael K., and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.”
Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 4–6,
doi:10.1016/j.ceb.2015.09.004.'
short: M.K. Sixt, E. Raz, Current Opinion in Cell Biology 36 (2015) 4–6.
date_created: 2018-12-11T11:53:25Z
date_published: 2015-10-01T00:00:00Z
date_updated: 2021-01-12T06:52:27Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/j.ceb.2015.09.004
intvolume: ' 36'
issue: '10'
language:
- iso: eng
month: '10'
oa_version: None
page: 4 - 6
publication: Current Opinion in Cell Biology
publication_status: published
publisher: Elsevier
publist_id: '5473'
scopus_import: 1
status: public
title: 'Editorial overview: Cell adhesion and migration'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 36
year: '2015'
...
---
_id: '1687'
abstract:
- lang: eng
text: Guided cell movement is essential for development and integrity of animals
and crucially involved in cellular immune responses. Leukocytes are professional
migratory cells that can navigate through most types of tissues and sense a wide
range of directional cues. The responses of these cells to attractants have been
mainly explored in tissue culture settings. How leukocytes make directional decisions
in situ, within the challenging environment of a tissue maze, is less understood.
Here we review recent advances in how leukocytes sense chemical cues in complex
tissue settings and make links with paradigms of directed migration in development
and Dictyostelium discoideum amoebae.
author:
- first_name: Milka
full_name: Sarris, Milka
last_name: Sarris
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Sarris M, Sixt MK. Navigating in tissue mazes: Chemoattractant interpretation
in complex environments. Current Opinion in Cell Biology. 2015;36(10):93-102.
doi:10.1016/j.ceb.2015.08.001'
apa: 'Sarris, M., & Sixt, M. K. (2015). Navigating in tissue mazes: Chemoattractant
interpretation in complex environments. Current Opinion in Cell Biology.
Elsevier. https://doi.org/10.1016/j.ceb.2015.08.001'
chicago: 'Sarris, Milka, and Michael K Sixt. “Navigating in Tissue Mazes: Chemoattractant
Interpretation in Complex Environments.” Current Opinion in Cell Biology.
Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.08.001.'
ieee: 'M. Sarris and M. K. Sixt, “Navigating in tissue mazes: Chemoattractant interpretation
in complex environments,” Current Opinion in Cell Biology, vol. 36, no.
10. Elsevier, pp. 93–102, 2015.'
ista: 'Sarris M, Sixt MK. 2015. Navigating in tissue mazes: Chemoattractant interpretation
in complex environments. Current Opinion in Cell Biology. 36(10), 93–102.'
mla: 'Sarris, Milka, and Michael K. Sixt. “Navigating in Tissue Mazes: Chemoattractant
Interpretation in Complex Environments.” Current Opinion in Cell Biology,
vol. 36, no. 10, Elsevier, 2015, pp. 93–102, doi:10.1016/j.ceb.2015.08.001.'
short: M. Sarris, M.K. Sixt, Current Opinion in Cell Biology 36 (2015) 93–102.
date_created: 2018-12-11T11:53:28Z
date_published: 2015-10-01T00:00:00Z
date_updated: 2021-01-12T06:52:31Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.ceb.2015.08.001
ec_funded: 1
file:
- access_level: open_access
checksum: c29973924b790aab02fdd91857759cfb
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:21Z
date_updated: 2020-07-14T12:45:12Z
file_id: '4875'
file_name: IST-2016-445-v1+1_1-s2.0-S0955067415001064-main.pdf
file_size: 797964
relation: main_file
file_date_updated: 2020-07-14T12:45:12Z
has_accepted_license: '1'
intvolume: ' 36'
issue: '10'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: 93 - 102
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Current Opinion in Cell Biology
publication_status: published
publisher: Elsevier
publist_id: '5458'
pubrep_id: '445'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Navigating in tissue mazes: Chemoattractant interpretation in complex environments'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 36
year: '2015'
...
---
_id: '1686'
author:
- first_name: Eva
full_name: Kiermaier, Eva
id: 3EB04B78-F248-11E8-B48F-1D18A9856A87
last_name: Kiermaier
orcid: 0000-0001-6165-5738
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Kiermaier E, Sixt MK. Fragmented communication between immune cells: Neutrophils
blaze a trail with migratory cues for T cells to follow to sites of infection.
Science. 2015;349(6252):1055-1056. doi:10.1126/science.aad0867'
apa: 'Kiermaier, E., & Sixt, M. K. (2015). Fragmented communication between
immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow
to sites of infection. Science. American Association for the Advancement
of Science. https://doi.org/10.1126/science.aad0867'
chicago: 'Kiermaier, Eva, and Michael K Sixt. “Fragmented Communication between
Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow
to Sites of Infection.” Science. American Association for the Advancement
of Science, 2015. https://doi.org/10.1126/science.aad0867.'
ieee: 'E. Kiermaier and M. K. Sixt, “Fragmented communication between immune cells:
Neutrophils blaze a trail with migratory cues for T cells to follow to sites of
infection,” Science, vol. 349, no. 6252. American Association for the Advancement
of Science, pp. 1055–1056, 2015.'
ista: 'Kiermaier E, Sixt MK. 2015. Fragmented communication between immune cells:
Neutrophils blaze a trail with migratory cues for T cells to follow to sites of
infection. Science. 349(6252), 1055–1056.'
mla: 'Kiermaier, Eva, and Michael K. Sixt. “Fragmented Communication between Immune
Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to
Sites of Infection.” Science, vol. 349, no. 6252, American Association
for the Advancement of Science, 2015, pp. 1055–56, doi:10.1126/science.aad0867.'
short: E. Kiermaier, M.K. Sixt, Science 349 (2015) 1055–1056.
date_created: 2018-12-11T11:53:28Z
date_published: 2015-09-04T00:00:00Z
date_updated: 2021-01-12T06:52:31Z
day: '04'
department:
- _id: MiSi
doi: 10.1126/science.aad0867
intvolume: ' 349'
issue: '6252'
language:
- iso: eng
month: '09'
oa_version: None
page: 1055 - 1056
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5459'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Fragmented communication between immune cells: Neutrophils blaze a trail with
migratory cues for T cells to follow to sites of infection'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 349
year: '2015'
...
---
_id: '477'
abstract:
- lang: eng
text: Dendritic cells are potent antigen-presenting cells endowed with the unique
ability to initiate adaptive immune responses upon inflammation. Inflammatory
processes are often associated with an increased production of serotonin, which
operates by activating specific receptors. However, the functional role of serotonin
receptors in regulation of dendritic cell functions is poorly understood. Here,
we demonstrate that expression of serotonin receptor 5-HT7 (5-HT7TR) as well as
its downstream effector Cdc42 is upregulated in dendritic cells upon maturation.
Although dendritic cell maturation was independent of 5-HT7TR, receptor stimulation
affected dendritic cell morphology through Cdc42-mediated signaling. In addition,
basal activity of 5-HT7TR was required for the proper expression of the chemokine
receptor CCR7, which is a key factor that controls dendritic cell migration. Consistent
with this, we observed that 5-HT7TR enhances chemotactic motility of dendritic
cells in vitro by modulating their directionality and migration velocity. Accordingly,
migration of dendritic cells in murine colon explants was abolished after pharmacological
receptor inhibition. Our results indicate that there is a crucial role for 5-HT7TR-Cdc42-mediated
signaling in the regulation of dendritic cell morphology and motility, suggesting
that 5-HT7TR could be a new target for treatment of a variety of inflammatory
and immune disorders.
author:
- first_name: Katrin
full_name: Holst, Katrin
last_name: Holst
- first_name: Daria
full_name: Guseva, Daria
last_name: Guseva
- first_name: Susann
full_name: Schindler, Susann
last_name: Schindler
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Armin
full_name: Braun, Armin
last_name: Braun
- first_name: Himpriya
full_name: Chopra, Himpriya
last_name: Chopra
- first_name: Oliver
full_name: Pabst, Oliver
last_name: Pabst
- first_name: Evgeni
full_name: Ponimaskin, Evgeni
last_name: Ponimaskin
citation:
ama: Holst K, Guseva D, Schindler S, et al. The serotonin receptor 5-HT7R regulates
the morphology and migratory properties of dendritic cells. Journal of Cell
Science. 2015;128(15):2866-2880. doi:10.1242/jcs.167999
apa: Holst, K., Guseva, D., Schindler, S., Sixt, M. K., Braun, A., Chopra, H., …
Ponimaskin, E. (2015). The serotonin receptor 5-HT7R regulates the morphology
and migratory properties of dendritic cells. Journal of Cell Science. Company
of Biologists. https://doi.org/10.1242/jcs.167999
chicago: Holst, Katrin, Daria Guseva, Susann Schindler, Michael K Sixt, Armin Braun,
Himpriya Chopra, Oliver Pabst, and Evgeni Ponimaskin. “The Serotonin Receptor
5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.”
Journal of Cell Science. Company of Biologists, 2015. https://doi.org/10.1242/jcs.167999.
ieee: K. Holst et al., “The serotonin receptor 5-HT7R regulates the morphology
and migratory properties of dendritic cells,” Journal of Cell Science,
vol. 128, no. 15. Company of Biologists, pp. 2866–2880, 2015.
ista: Holst K, Guseva D, Schindler S, Sixt MK, Braun A, Chopra H, Pabst O, Ponimaskin
E. 2015. The serotonin receptor 5-HT7R regulates the morphology and migratory
properties of dendritic cells. Journal of Cell Science. 128(15), 2866–2880.
mla: Holst, Katrin, et al. “The Serotonin Receptor 5-HT7R Regulates the Morphology
and Migratory Properties of Dendritic Cells.” Journal of Cell Science,
vol. 128, no. 15, Company of Biologists, 2015, pp. 2866–80, doi:10.1242/jcs.167999.
short: K. Holst, D. Guseva, S. Schindler, M.K. Sixt, A. Braun, H. Chopra, O. Pabst,
E. Ponimaskin, Journal of Cell Science 128 (2015) 2866–2880.
date_created: 2018-12-11T11:46:41Z
date_published: 2015-06-15T00:00:00Z
date_updated: 2021-01-12T08:00:54Z
day: '15'
department:
- _id: MiSi
doi: 10.1242/jcs.167999
intvolume: ' 128'
issue: '15'
language:
- iso: eng
month: '06'
oa_version: None
page: 2866 - 2880
publication: Journal of Cell Science
publication_status: published
publisher: Company of Biologists
publist_id: '7343'
quality_controlled: '1'
scopus_import: 1
status: public
title: The serotonin receptor 5-HT7R regulates the morphology and migratory properties
of dendritic cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 128
year: '2015'
...