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10.1097/PPO.0000000000000059

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C4151049!4151049!25098287
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suck abstract from ncbi


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pmid25098287      Cancer+J 2014 ; 20 (4): 265-71
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  • Biochemical Signaling of PD-1 on T Cells and Its Functional Implications #MMPMID25098287
  • Boussiotis VA; Chatterjee P; Li L
  • Cancer J 2014[Jul]; 20 (4): 265-71 PMID25098287show ga
  • Maintenance of peripheral tolerance is essential for homeostasis of the immune system. While central tolerance mechanisms result in deletion of the majority of self-reactive T cells, T lymphocytes specific for self-antigens also escape this process and circulate in the periphery. To control the development of autoimmunity, multiple mechanisms of peripheral tolerance have evolved, including T cell anergy, deletion and suppression by regulatory T cells (Treg). The pathway consisting of the PD-1 receptor (CD279) and its ligands PD-L1 (B7-H1, CD274) and PD-L2 (B7-DC; CD273) plays a vital role in the induction and maintenance of peripheral tolerance. This pathway also regulates the balance between stimulatory and inhibitory signals needed for effective immunity and maintenance of T cell homeostasis. In contrast to this important beneficial role in maintaining T cell homeostasis, PD-1 mediates potent inhibitory signals that prevent the expansion and function of T effector cells and have detrimental effects on anti-viral and anti-tumor immunity. In spite of the compelling studies on the significant functional role of PD-1 in mediating inhibition of activated T cells, little is known about how PD-1 blocks T cell activation. Here, we will provide a brief overview of the signaling events that are regulated by PD-1 triggering and we will discuss their implications on cell intrinsic and extrinsic mechanisms that determine the fate and function of T effector cells.
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