---
_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'
...