| First Author | Kishore M | Year | 2012 |
| Journal | PLoS One | Volume | 7 |
| Issue | 6 | Pages | e39433 |
| PubMed ID | 22724015 | Mgi Jnum | J:187814 |
| Mgi Id | MGI:5438415 | Doi | 10.1371/journal.pone.0039433 |
| Citation | Kishore M, et al. (2012) Primed T cell responses to chemokines are regulated by the immunoglobulin-like molecule CD31. PLoS One 7(6):e39433 |
| abstractText | CD31, an immunoglobulin-like molecule expressed by leukocytes and endothelial cells, is thought to contribute to the physiological regulation T cell homeostasis due to the presence of two immunotyrosine-based inhibitory motifs in its cytoplasmic tail. Indeed, loss of CD31 expression leads to uncontrolled T cell-mediated inflammation in a variety of experimental models of disease and certain CD31 polymorphisms correlate with increased disease severity in human graft-versus-host disease and atherosclerosis. The molecular mechanisms underlying CD31-mediated regulation of T cell responses have not yet been clarified. We here show that CD31-mediated signals attenuate T cell chemokinesis both in vitro and in vivo. This effect selectively affects activated/memory T lymphocytes, in which CD31 is clustered on the cell membrane where it segregates to the leading edge. We provide evidence that this molecular segregation, which does not occur in naive T lymphocytes, might lead to cis-CD31 engagement on the same membrane and subsequent interference with the chemokine-induced PI3K/Akt signalling pathway. We propose that CD31-mediated modulation of memory T cell chemokinesis is a key mechanism by which this molecule contributes to the homeostatic regulation of effector T cell immunity. |
