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Recently, several reports have suggested that innate immune systems such as interferon\u2010\u03b1 (IFN\u2010\u03b1)\u2010producing plasmacytoid dendritic cells and NOD\u2010like receptor family pyrin domain\u2010containing protein 3 (NLRP3) inflammasomes play a role in the pathogenesis of AA. However, critical studies about their involvement in the initiation of AA have not yet been reported. Therefore, we investigated the expression of innate immune cytokines in serum and skin, and examined the effect of a selective NLRP3 inhibitor, MCC950, on AA in C3H\/HeJ mice, induced by transferring cultured skin\u2010draining lymph node cells. IFN\u2010\u03b1 production was upregulated in lesions of AA\u2010affected mice, and interleukin\u20101\u03b2 in serum and skin was highly expressed before onset as well as postonset. Furthermore, MCC950 treatment prevented AA development and promoted hair growth in AA mouse models by reducing NLRP3\u00a0signalling and Th1\/Tc1 chemokines and cytokines in the skin. These results suggest that NLRP3 inflammasome contributes to AA onset and chronicity, and NLRP3 inhibitor may be a potential therapeutic agent for AA.<\/jats:p>","DOI":"10.1111\/exd.14432","type":"journal-article","created":{"date-parts":[[2021,7,16]],"date-time":"2021-07-16T18:32:17Z","timestamp":1626460337000},"page":"133-142","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["NLRP3 inflammasome activation contributes to development of alopecia areata in C3H\/HeJ mice"],"prefix":"10.1111","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9089-1227","authenticated-orcid":false,"given":"Kei","family":"Hashimoto","sequence":"first","affiliation":[{"name":"Kyoto R&amp;D Center Maruho Co., Ltd. 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