白色念珠菌
自身免疫调节因子
自身免疫
RAR相关孤儿受体γ
免疫学
慢性皮肤黏膜念珠菌病
生物
先天性淋巴细胞
免疫系统
调节器
白色体
获得性免疫系统
T细胞
微生物学
基因
FOXP3型
医学
遗传学
疾病
内科学
作者
Jan Dobeš,Osher Ben-Nun,Amit Binyamin,Liat Stoler-Barak,Bergithe E. Oftedal,Yael Goldfarb,Noam Kadouri,Yael Gruper,Tal Givony,Itay Zalayat,Katarína Kováčová,Helena Böhmová,Evgeny Valter,Ziv Shulman,Dominik Filipp,Eystein S. Husebye,Jakub Abramson
标识
DOI:10.1038/s41590-022-01247-6
摘要
Patients with loss of function in the gene encoding the master regulator of central tolerance AIRE suffer from a devastating disorder called autoimmune polyendocrine syndrome type 1 (APS-1), characterized by a spectrum of autoimmune diseases and severe mucocutaneous candidiasis. Although the key mechanisms underlying the development of autoimmunity in patients with APS-1 are well established, the underlying cause of the increased susceptibility to Candida albicans infection remains less understood. Here, we show that Aire+MHCII+ type 3 innate lymphoid cells (ILC3s) could sense, internalize and present C. albicans and had a critical role in the induction of Candida-specific T helper 17 (TH17) cell clones. Extrathymic Rorc-Cre-mediated deletion of Aire resulted in impaired generation of Candida-specific TH17 cells and subsequent overgrowth of C. albicans in the mucosal tissues. Collectively, our observations identify a previously unrecognized regulatory mechanism for effective defense responses against fungal infections.
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