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- W1558018911 abstract "Abstract Necroptosis is a form of programed cell death, in which receptor-interacting protein (RIP)1 and subsequent RIP3 kinase activation is a central pathway for its development. Necroptotic cells induce inflammation through the release of various cytokines or necrotic danger-associated molecular patterns. Recent reports indicated that mice with keratinocyte-specific necroptotic cell death exhibit severe chronic skin inflammation, which suggests the involvement of necroptosis in the pathogenesis of chronic skin inflammatory diseases, such as psoriasis. In this study, we investigated the involvement of necroptosis in the pathogenesis of psoriasis using an imiquimod (IMQ)-induced mouse psoriasis model. Daily application of IMQ to skin caused skin inflammation with psoriariform scaly erythema with epidermal and dermal thickening. In the skin, we detected positive signals of TUNEL both in the epidermis and dermis, suggesting the induction of programmed cell death in skin by IMQ application. In addition, RIP3 expression was significantly upregulated both in mRNA and protein level in the skin lesions. Administration of necrostatin-1, a specific inhibitor of RIP1 kinase, significantly reduced the severity of IMQ-induced psoriasis-like dermatitis. Immunohistochemical analysis revealed positive signals for RIP3 in the human psoriasis skin lesion. These results indicate the involvement of necroptosis in mouse psoriasis model, and suggest it's involvement in the pathogenesis of psoriasis." @default.
- W1558018911 created "2016-06-24" @default.
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- W1558018911 date "2014-05-01" @default.
- W1558018911 modified "2023-09-26" @default.
- W1558018911 title "Involvement of necroptosis in the development of imiquimod-induced psoriasis-like dermatitis (BA3P.135)" @default.
- W1558018911 doi "https://doi.org/10.4049/jimmunol.192.supp.44.5" @default.
- W1558018911 hasPublicationYear "2014" @default.
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