PD‐1 inhibits T‐cell receptor induced phosphorylation of the ZAP70/CD3ζ signalosome and downstream signaling to PKCθ

By K. Sheppard, L. Fitz, Julie Lee, Christina Benander, Judith A George, J. Wooters, Yongchang Qiu, J. Jussif, Laura L. Carter, C. Wood and 1 more. 2004

679 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/5c28199e8825b441a0109a59c898d03fdb938b45

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Citations in the corpus

PD-1 and its ligands in tolerance and immunity. (2008, background): “Two phosphatases, SH2-domain containing tyrosine phosphatase 1 (SHP-1) and SHP-2, can bind to the ITIM and ITSM motifs of PD-1 (35, 36).”
Programmed cell death 1 forms negative costimulatory microclusters that directly inhibit T cell receptor signaling by recruiting phosphatase SHP2 (2012, background): “CD28–PKC-–CARMA-1 axis or other pathways that associate with the c-SMAC.”
Bioenergetic insufficiencies due to metabolic alterations regulated by PD-1 are an early driver of CD8+ T cell exhaustion (2016, background): “Engagement of PD-1 by its ligand PD-L1 results 358 Immunity 45, 358–373, August 16, 2016 ª 2016 Elsevier Inc. in the formation of microclusters with the TCR (Yokosuka et al., 2012) and PD-1 inhibits proximal signaling molecules after TCR engagement (Sheppard et al., 2004).”
PD-1 is a regulator of virus-specific CD8+ T cell survival in HIV infection (2006, background): “In support of this negative role, in vitro studies using primary human T cells have shown that PD-1 ligation can inhibit TCR-mediated signaling by reducing phosphorylation of ZAP70, activation of PKCθ ( 22 ), and activation of Akt (23).”