Imperial College London
Portrait Picture

Professor Guido Franzoso

Faculty of Medicine, Department of Immunology and Inflammation

Chair in Inflammation and Signal Transduction
 
 
 
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Contact

 

+44 (0)20 3313 8421g.franzoso Website

 
 
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Assistant

 

Miss Anjli Jagpal +44 (0)20 3313 3152

 
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Location

 

5N1Commonwealth BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Ma:2010:10.1073/pnas.1011748107,
author = {Ma, L and Mauro, C and Cornish, GH and Chai, JG and Coe, D and Fu, H and Patton, D and Okkenhaug, K and Franzoso, G and Dyson, J and Nourshargh, S and Marelli-Berg, FM},
doi = {10.1073/pnas.1011748107},
journal = {Proceedings of the National Academy of Sciences of USA},
pages = {19461--19466},
title = {Ig gene-like molecule CD31 plays a nonredundant role in the regulation of T-cell immunity and tolerance.},
url = {http://dx.doi.org/10.1073/pnas.1011748107},
volume = {107},
year = {2010}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - CD31 is an Ig-like molecule expressed by leukocytes and endothelial cells with an established role in the regulation of leukocyte trafficking. Despite genetic deletion of CD31 being associated with exacerbation of T cell-mediated autoimmunity, the contribution of this molecule to T-cell responses is largely unknown. Here we report that tumor and allograft rejection are significantly enhanced in CD31-deficient mice, which are also resistant to tolerance induction. We propose that these effects are dependent on an as yet unrecognized role for CD31-mediated homophilic interactions between T cells and antigen-presenting cells (APCs) during priming. We show that loss of CD31 interactions leads to enhanced primary clonal expansion, increased killing capacity, and diminished regulatory functions by T cells. Immunomodulation by CD31 signals correlates with a partial inhibition of proximal T-cell receptor (TCR) signaling, specifically Zap-70 phosphorylation. However, CD31-deficient mice do not develop autoimmunity due to increased T-cell death following activation, and we show that CD31 triggering induces Erk-mediated prosurvival activity in T cells either in conjunction with TCR signaling or autonomously. We conclude that CD31 functions as a nonredundant comodulator of T-cell responses, which specializes in sizing the ensuing immune response by setting the threshold for T-cell activation and tolerance, while preventing memory T-cell death.
AU  - Ma,L
AU  - Mauro,C
AU  - Cornish,GH
AU  - Chai,JG
AU  - Coe,D
AU  - Fu,H
AU  - Patton,D
AU  - Okkenhaug,K
AU  - Franzoso,G
AU  - Dyson,J
AU  - Nourshargh,S
AU  - Marelli-Berg,FM
DO  - 10.1073/pnas.1011748107
EP  - 19466
PY  - 2010///
SN  - 0027-8424
SP  - 19461
TI  - Ig gene-like molecule CD31 plays a nonredundant role in the regulation of T-cell immunity and tolerance.
T2  - Proceedings of the National Academy of Sciences of USA
UR  - http://dx.doi.org/10.1073/pnas.1011748107
UR  - https://www.pnas.org/doi/full/10.1073/pnas.1011748107
UR  - http://hdl.handle.net/10044/1/99652
VL  - 107
ER  -
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