| First Author | Singh MD | Year | 2018 |
| Journal | J Exp Med | Volume | 215 |
| Issue | 9 | Pages | 2429-2443 |
| PubMed ID | 30093532 | Mgi Jnum | J:266280 |
| Mgi Id | MGI:6201983 | Doi | 10.1084/jem.20171820 |
| Citation | Singh MD, et al. (2018) B cell adaptor for PI3-kinase (BCAP) modulates CD8(+) effector and memory T cell differentiation. J Exp Med 215(9):2429-2443 |
| abstractText | CD8(+) T cells respond to signals via the T cell receptor (TCR), costimulatory molecules, and immunoregulatory cytokines by developing into diverse populations of effector and memory cells. The relative strength of phosphoinositide 3-kinase (PI3K) signaling early in the T cell response can dramatically influence downstream effector and memory T cell differentiation. We show that initial PI3K signaling during T cell activation results in up-regulation of the signaling scaffold B cell adaptor for PI3K (BCAP), which further potentiates PI3K signaling and promotes the accumulation of CD8(+) T cells with a terminally differentiated effector phenotype. Accordingly, BCAP-deficient CD8(+) T cells have attenuated clonal expansion and altered effector and memory T cell development following infection with Listeria monocytogenes Thus, induction of BCAP serves as a positive feedback circuit to enhance PI3K signaling in activated CD8(+) T cells, thereby acting as a molecular checkpoint regulating effector and memory T cell development. |
