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• W3092900611 abstract "Abstract Use of immune checkpoint inhibitors that target programmed cell death-1 (PD-1) can lead to various autoimmune-related adverse events (irAEs) including psoriasis-like dermatitis. Our observations on human samples indicated enhanced epidermal infiltration of CD8 T cells, and the pathogenesis of which appears to be dependent on IL-6 in the PD-1 signal blockade-induced psoriasis-like dermatitis. By using a murine model of imiquimod-induced psoriasis-like dermatitis, we further demonstrated that PD-1 deficiency accelerates skin inflammation with activated cytotoxic CD8 T cells into the epidermis, which engage in pathogenic cross-talk with keratinocytes resulting in production of IL-6. Moreover, genetically modified mice lacking PD-1 expression only on CD8 T cells developed accelerated dermatitis, moreover, blockade of IL-6 signaling by anti-IL-6 receptor antibody could ameliorate the dermatitis. Collectively, PD-1 signal blockade-induced psoriasis-like dermatitis is mediated by PD-1 signaling on CD8 T cells, and furthermore, IL-6 is likely to be a therapeutic target for the dermatitis." @default.
• W3092900611 created "2020-10-22" @default.
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• W3092900611 date "2020-10-15" @default.
• W3092900611 modified "2023-10-16" @default.
• W3092900611 title "Activation of CD8 T cells accelerates anti-PD-1 antibody-induced psoriasis-like dermatitis through IL-6" @default.
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• W3092900611 doi "https://doi.org/10.1038/s42003-020-01308-2" @default.
• W3092900611 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7567105" @default.
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• W3092900611 hasPublicationYear "2020" @default.
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