부산대학교 도서관

Patients with loss of function in the gene encoding the master regulator of central tolerance AIREsuffer 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 albicansinfection remains less understood. Here, we show that Aire+MHCII+type 3 innate lymphoid cells (ILC3s) could sense, internalize and present C. albicansand had a critical role in the induction of Candida-specific T helper 17 (TH17) cell clones. Extrathymic Rorc-Cre-mediated deletion of Aireresulted in impaired generation of Candida-specific TH17 cells and subsequent overgrowth of C. albicansin the mucosal tissues. Collectively, our observations identify a previously unrecognized regulatory mechanism for effective defense responses against fungal infections.