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• W2619512349 abstract "Programmed cell death ligand-1 (PD-L1) is typically produced by cancer cells and suppresses immunity through the receptor PD-1 expressed on T cells. However, the role of PD-L1 and PD-1 in regulating pain and neuronal function is unclear. Here we report that both melanoma and normal neural tissues including dorsal root ganglion (DRG) produce PD-L1 that can potently inhibit acute and chronic pain. Intraplantar injection of PD-L1 evoked analgesia in naive mice via PD-1, whereas PD-L1 neutralization or PD-1 blockade induced mechanical allodynia. Mice lacking Pd1 (Pdcd1) exhibited thermal and mechanical hypersensitivity. PD-1 activation in DRG nociceptive neurons by PD-L1 induced phosphorylation of the tyrosine phosphatase SHP-1, inhibited sodium channels and caused hyperpolarization through activation of TREK2 K+ channels. PD-L1 also potently suppressed nociceptive neuron excitability in human DRGs. Notably, blocking PD-L1 or PD-1 elicited spontaneous pain and allodynia in melanoma-bearing mice. Our findings identify a previously unrecognized role of PD-L1 as an endogenous pain inhibitor and a neuromodulator." @default.
• W2619512349 created "2017-06-05" @default.
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• W2619512349 date "2017-05-22" @default.
• W2619512349 modified "2023-10-03" @default.
• W2619512349 title "PD-L1 inhibits acute and chronic pain by suppressing nociceptive neuron activity via PD-1" @default.
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• W2619512349 doi "https://doi.org/10.1038/nn.4571" @default.
• W2619512349 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6827979" @default.
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