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首页> 外文期刊>The Journal of Experomental Medicine >B cell adaptor for PI3-kinase (BCAP) modulates CD8 + effector and memory T cell differentiation
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B cell adaptor for PI3-kinase (BCAP) modulates CD8 + effector and memory T cell differentiation

机译：PI3-激酶（BCAP）的B细胞衔接子调节CD8 + 效应子和记忆T细胞分化

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Singh et al. show that expression of B cell adaptor for PI3-kinase (BCAP) is induced upon T cell activation and that this helps control effector and memory CD8 ~(+) T cell differentiation. 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.
机译：辛格等。结果表明，在T细胞活化后诱导了PI3激酶（BCAP）的B细胞衔接子的表达，这有助于控制效应子和记忆CD8〜（+）T细胞的分化。 CD8〜（+）T细胞通过发展为效应细胞和记忆细胞的不同群体，通过T细胞受体（TCR），共刺激分子和免疫调节细胞因子对信号作出反应。在T细胞反应早期，磷酸肌醇3激酶（PI3K）信号的相对强度可以极大地影响下游效应子和记忆T细胞的分化。我们显示，在T细胞活化过程中，初始PI3K信号传导导致PI3K（BCAP）信号传导支架B细胞适配器的上调，这进一步增强了PI3K信号传导，并促进CD8〜（+）T细胞的积累，并带有终末分化的效应子。表型。因此，感染单核细胞增生性李斯特菌后，BCAP缺陷型CD8〜（+）T细胞的克隆扩增能力减弱，效应子和记忆T细胞发育改变。因此，BCAP的诱导充当正反馈电路，以增强活化的CD8〜（+）T细胞中的PI3K信号传导，从而充当调节效应子和记忆T细胞发育的分子检查点。

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