SHP-1 and SHP-2 Associate with Immunoreceptor Tyrosine-Based Switch Motif of Programmed Death 1 upon Primary Human T Cell Stimulation, but Only Receptor Ligation Prevents T Cell Activation1

By J. Chemnitz, R. Parry, K. Nichols, C. June, J. Riley. Journal of Immunology, 2004

1,222 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/1430485c055ac8dcbf2a97da8662ead5f0bfeaf7

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Citations in the corpus

Blockade of B7-H1 and PD-1 by monoclonal antibodies potentiates cancer therapeutic immunity. (2005, background): “Interestingly, a recent study indicates that PD-1 colocalization with TCR is required for its inhibitory function (37), suggesting that B7-H1 on tumor cells may directly bind to PD-1 to prevent TCR-mediated recognition or signaling function.”
LAG3 (CD223) as a Cancer Immunotherapy Target (2017, background): “These motifs are often used by other IRs to engage Src homology 2 (SH2) domain-containing protein tyrosine phosphatases, such as (SHP)-1/2 that are used by PD1 to limit TCR signaling (21).”
CTLA-4 and PD-1 Receptors Inhibit T-Cell Activation by Distinct Mechanisms (2004, methodology): “Despite the shared ability to block T-cell activation, the cytoplasmic domain of PD-1 shows significant differences from CTLA-4 by encoding both an immunoreceptor tyrosinebased inhibitory motif (ITIM) and an immunoreceptor tyrosine-based switch motif (ITSM), of which the ITSM appears to be the most ”
PD-1 and its ligands in tolerance and immunity. (2008, background): “CD150 association with either the SH2-containing inositol phosphatase or the SH2-containing protein tyrosine phosphatase is regulated by the adaptor protein SH2D1A.”
Control of peripheral T‐cell tolerance and autoimmunity via the CTLA‐4 and PD‐1 pathways (2008, background): “PD1 has both an immunoreceptor tyrosine-based inhibitory motif (ITIM) as well as an immunoreceptor tyrosine-based switch motif (ITSM) (67).”
Programmed cell death 1 forms negative costimulatory microclusters that directly inhibit T cell receptor signaling by recruiting phosphatase SHP2 (2012, background): “…an immunological synapse because AND-TCR Tg Pdcd1 / Rag2 / cells expressing Y225F, Y248F, or YFYF mutant PD-1 formed a higher percentage of stable synapses than WT: WT, 40%; Y225F, 50%; Y248F, 58%; YFYF, 80%; and WT without PD-L1-GPI, 94% of SHP2 (Okazaki et al., 2001; Chemnitz et al., 2004).”
Anti-PD-1 and Anti-CTLA-4 Therapies in Cancer: Mechanisms of Action, Efficacy, and Limitations (2018, background): “By interfering with early TCR/CD28 signaling and associated IL-2-dependent positive feedback, PD-1 signaling therefore results in reduced cytokine production [such as IL-2, IFN-γ, and tumor necrosis factor (TNF)-α], cell cycle progression, and pro-survival Bcl-xL gene expression, as well as reduced ”
PD-1 signaling in primary T cells (2009, background): “are blocked, including PI3K activation (26, 42).”