| First Author | Vazquez-Cintron EJ | Year | 2012 |
| Journal | PLoS One | Volume | 7 |
| Issue | 5 | Pages | e36101 |
| PubMed ID | 22567129 | Mgi Jnum | J:187262 |
| Mgi Id | MGI:5435992 | Doi | 10.1371/journal.pone.0036101 |
| Citation | Vazquez-Cintron EJ, et al. (2012) Protocadherin-18 is a novel differentiation marker and an inhibitory signaling receptor for CD8+ effector memory T cells. PLoS One 7(5):e36101 |
| abstractText | CD8(+) tumor infiltrating T cells (TIL) lack effector-phase functions due to defective proximal TCR-mediated signaling previously shown to result from inactivation of p56(lck) kinase. We identify a novel interacting partner for p56(lck) in nonlytic TIL, Protocadherin-18 ('pcdh18'), and show that pcdh18 is transcribed upon in vitro or in vivo activation of all CD8(+) central memory T cells (CD44(+)CD62L(hi)CD127(+)) coincident with conversion into effector memory cells (CD44(+)CD62L(lo)CD127(+)). Expression of pcdh18 in primary CD8(+) effector cells induces the phenotype of nonlytic TIL: defective proximal TCR signaling, cytokine secretion, and cytolysis, and enhanced AICD. pcdh18 contains a motif (centered at Y842) shared with src kinases (QGQYQP) that is required for the inhibitory phenotype. Thus, pcdh18 is a novel activation marker of CD8(+) memory T cells that can function as an inhibitory signaling receptor and restrict the effector phase. |
