PD-1 immunoreceptor inhibits B cell receptor-mediated signaling by recruiting src homology 2-domain-containing tyrosine phosphatase 2 to phosphotyrosine

By Taku Okazaki, A. Maeda, Hiroyuki Nishimura, T. Kurosaki, Tasuku Honjo. Proceedings of the National Academy of Sciences of the United States of America, 2001

824 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/66afc38faf024e5263229ca2cf3eb0a0f1192409

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Citations in the corpus

The PD-1 Pathway in Tolerance and Autoimmunity (2010, background): “Mutagenesis studies indicate that the tyrosine within the ITSM motif is essential for PD-1 function in T cells and B cells (17, 18).”
Programmed cell death 1 forms negative costimulatory microclusters that directly inhibit T cell receptor signaling by recruiting phosphatase SHP2 (2012, background): “As shown previously, SHP2 was recruited to PD-1 upon the PD-1–PD-L1 or –PD-L2 binding, whereas the PD-1–SHP1 association remained at background level (Fig.”
PD-1 signaling in primary T cells (2009, background): “We and others have shown that PD-1 is quite functional when it contains just a single tyrosine molecule (26, 46).”
T cell exhaustion (2011, background): “In contrast, inhibitory motif–containing molecules such as PD-1 can recruit phosphatases (such as SHP-1, SHP-2 or SHIP) to TCR-proximal signaling complexes and attenuate signalin”
CTLA-4 and PD-1 Receptors Inhibit T-Cell Activation by Distinct Mechanisms (2004, background): “To date, all reports that specifically target PD-1 using PD-1 antibody (Ab) have shown that PD-1 acts as a negative regulator of T-cell activation (5, 47).”
Neoadjuvant checkpoint blockade for cancer immunotherapy (2020, result): “The expansion of B cells after anti–PD-1 therapy is consistent with the original basic functional description of the PD-1 pathway (70); however, their increased detection in the TME does not necessarily equate with a requirement for tumor rejection.”
Control of peripheral T‐cell tolerance and autoimmunity via the CTLA‐4 and PD‐1 pathways (2008, background): “PD-1 signaling can cause a redistribution of uniform cell surface expression to the immunological synapse and may potentially bring SHP1 and SHP2 with it (68, 69).”
Interaction of PD-L1 on tumor cells with PD-1 on tumor-specific T cells as a mechanism of immune evasion: implications for tumor immunotherapy (2005, background): “However, SHP-2 recruitment to the C-terminal phosphotyrosine and the N-terminal tyrosine residue is almost dispensable for the inhibitory effects of PD-1, raising questions about the precise biochemical mechanism of this effect [50].”
PD-L1/B7H-1 Inhibits the Effector Phase of Tumor Rejection by T Cell Receptor (TCR) Transgenic CD8+ T Cells (2004, background): “The cytoplasmic tail contains an ITIM motif and can interact with the phosphatase SHP2 (16).”