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- W2802184218 abstract "The NLRP3 inflammasome plays a key role in sensing pathogens and danger signals in the innate immune system and is thought to be involved in oxidative stress-driven undesirable immune response of vitiligo, a common skin disease characterized by melanocyte destruction by CD8+ T cells. However, the mechanism by which the NLRP3 inflammasome activates and induces vitiligo is not clear. In this study, we revealed that NLRP3 and IL-1β expression increased in serum and lesions of patients with vitiligo, and serum IL-1β levels were positively correlated with disease activity. Furthermore, the H2O2-induced NLRP3 inflammasome activation in keratinocytes, which was due to the mitochondrial Ca2+ influx mediated by TRPM2 channels, could up-regulate chemotaxis-related proteins, including CXCL10 and CXCL16 secretion in keratinocytes, as well as T-cell activation and cytotoxic markers through IL-1β/IL-1R signal, and thus promoted chemotactic ability and cytotoxic functions of CD8+ T cells derived from patients with vitiligo. In Conclusion, our study first demonstrated that TRPM2 mediates NLRP3 inflammasome activation under oxidative stress in human keratinocytes, which aggravates CD8+ T-cell skin migration, activation and cytotoxic functions, and thereby contributes to dysregulated autoimmune response in patients with vitiligo." @default.
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- W2802184218 date "2018-05-01" @default.
- W2802184218 modified "2023-09-27" @default.
- W2802184218 title "910 TRPM2-dependent NLRP3 inflammasome activation exacerbates the oxidative stress-driven immune response in patients with vitiligo" @default.
- W2802184218 doi "https://doi.org/10.1016/j.jid.2018.03.922" @default.
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