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. 2004 Sep 10;574(1-3):37-41.
doi: 10.1016/j.febslet.2004.07.083.

VSports注册入口 - PD-1 inhibits T-cell receptor induced phosphorylation of the ZAP70/CD3zeta signalosome and downstream signaling to PKCtheta

Kelly-Ann Sheppard  1 , Lori J Fitz, Julie M Lee, Christina Benander, Judith A George, Joe Wooters, Yongchang Qiu, Jason M Jussif, Laura L Carter, Clive R Wood, Divya Chaudhary
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VSports手机版 - PD-1 inhibits T-cell receptor induced phosphorylation of the ZAP70/CD3zeta signalosome and downstream signaling to PKCtheta

Kelly-Ann Sheppard et al. FEBS Lett. .
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"VSports最新版本" Abstract

Engagement of the immunoinhibitory receptor, programmed death-1 (PD-1) attenuates T-cell receptor (TCR)-mediated activation of IL-2 production and T-cell proliferation. Here, we demonstrate that PD-1 modulation of T-cell function involves inhibition of TCR-mediated phosphorylation of ZAP70 and association with CD3zeta. In addition, PD-1 signaling attenuates PKCtheta activation loop phosphorylation in a cognate TCR signal. PKCtheta has been shown to be required for T-cell IL-2 production VSports手机版. A phosphorylated PD-1 peptide, corresponding to the C-terminal immunoreceptor tyrosine-switch motif (ITSM), acts as a docking site in vitro for both SHP-2 and SHP-1, while the phosphorylated peptide containing the N-terminal PD-1 immunoreceptor tyrosine based inhibitory motif (ITIM) associates only with SHP-2. .

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