Evidence map›Paper›PMID 20978210›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Ig gene-like molecule CD31 plays a nonredundant role in the regulation of T-cell immunity and tolerance.

Liang Ma, Claudio Mauro, Georgina H Cornish, Jian-Guo Chai, David Coe, Hongmei Fu, Daniel Patton, Klaus Okkenhaug, Guido Franzoso, Julian Dyson and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
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  4. CD31 as a probable responding and gate-keeping protein of the blood-brain barrier and the risk of Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Review
  5. Article
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  7. Article
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  9. Article
  10. Generation of PECAM-1 (CD31) conditional knockout mice.Genesis (New York, N.Y. : 2000) · 2020
    Article
  11. Article
  12. Dissecting the defects in the neonatal CD8Journal of leukocyte biology · 2019
    Review
  13. Article
  14. Review
  15. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

Liang MaSection of Immunobiology and Inflammation and Signal Transduction, Department of Medicine, Imperial College London, Hammersmith Hospital Campus, London W12 0NN, United Kingdom.
Claudio Mauro
Georgina H Cornish
Jian-Guo Chai
David Coe
Hongmei Fu
Daniel Patton
Klaus Okkenhaug
Guido Franzoso
Julian Dyson
Sussan Nourshargh
Federica M Marelli-Berg
Babraham Institute · GBHammersmith Hospital · GBImperial College London · GBWilliam Harvey Research Institute · GB

Funding

The NF-kB Target, Gadd45Beta, in Lymphocytes and LiverR01CA084040 · NCI · UNIVERSITY OF CHICAGO · PI FRANZOSO, GUIDO · 2000 to 2009
$2.6M
Biotechnology and Biological Sciences Research Council BB/C509890/1Biotechnology and Biological Sciences Research Council BB/E009867/1Biotechnology and Biological Sciences Research Council BB/F020732/1Biotechnology and Biological Sciences Research Council BBS/E/B/0000C236British Heart Foundation PG/05/136/19997British Heart Foundation RG/09/002British Heart Foundation RG/09/002/26425Cancer Research UK C26587/A8839NCI NIH HHS R01 CA084040Wellcome TrustWellcome Trust 081172/Z/06/Z
6 · The paper itself

Abstract

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.

Indexed as

Immune ToleranceAnimalsCell SurvivalClone CellsCytotoxicity, ImmunologicGenes, ImmunoglobulinImmunologic MemoryLymphocyte ActivationMiceMice, KnockoutPlatelet Endothelial Cell Adhesion Molecule-1T-LymphocytesPlatelet Endothelial Cell Adhesion Molecule-1

Identifiers

PMID20978210
PMCPMC2984185
OpenAlexW2144248027

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.