期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 215, 期 9, 页码 2429-2443出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20171820
关键词
-
资金
- National Institutes of Health [AI124693, AI113325]
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.
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