Journal
IMMUNOLOGICAL REVIEWS
Volume 229, Issue -, Pages 114-125Publisher
WILEY-BLACKWELL PUBLISHING, INC
DOI: 10.1111/j.1600-065X.2009.00767.x
Keywords
SHP-1; SHP-2; metabolism
Categories
Funding
- Abramson Family Research Cancer Institute
- NIH [AI080192, AI057838, CA113783]
- NATIONAL CANCER INSTITUTE [R01CA113783] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI057838, P01AI080192] Funding Source: NIH RePORTER
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Programmed death-1 (PD-1) is a cell surface molecule that regulates the adaptive immune response. Engagement of PD-1 by its ligands PD-L1 or PD-L2 transduces a signal that inhibits T-cell proliferation, cytokine production, and cytolytic function. While a great deal is known concerning the biologic roles PD-1 plays in regulating the primary immune response and in T-cell exhaustion, comparatively little is known regarding how PD-1 ligation alters signaling pathways. PD-1 ligation is known to inhibit membrane-proximal T-cell signaling events, while ligation of the related inhibitory molecule cytotoxic T-lymphocyte antigen-4 appears to target more downstream signaling pathways. A major obstacle to an in-depth understanding of PD-1 signaling is the lack of physiologic models in which to study signal transduction. This review focuses on: (i) signaling pathways altered by PD-1 ligation, (ii) factors recruited upon PD-1 phosphorylation, and (iii) exploring the hypothesis that PD-1 ligation induces distinct signals during various stages of immune-cell differentiation. Lastly, we describe models to dissect the function of the PD-1 cytoplasmic tail using primary cells in the absence of agonist antibodies.
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