Journal
NATURE IMMUNOLOGY
Volume 23, Issue 7, Pages 1098-+Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41590-022-01247-6
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Funding
- European Research Council [ERC-2016-CoG-724821]
- Israel Science Foundation [1796/16, 1819/21]
- Chan Zuckerberg Initiative
- Bill and Marika Glied and Family Fund
- Binational Science Foundation
- Pasteur-Weizmann Delegation
- Enoch Foundation
- Ruth and Samuel David Gameroff Family Foundation
- Erica Drake Fund
- Lilly Fulop Fund for Multiple Sclerosis Research
- Dean of Faculty Fellowship by Weizmann Institute of Science
- Weizmann Institute of Science - Czech Academy of Sciences Bilateral Fellowship by Czech Academy of Sciences
- Charles University PRIMUS grant [Primus/21/MED/003]
- Czech Science Foundation JUNIOR STAR grant [21-22435M]
- K.G. Jebsen Center for autoimmune disorders
- Norwegian Research Council
- Novo Nordisk Foundation
- Regional Health Authorities of Western Norway
- Grant Agency of the Czech Republic [17-25365S]
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Research has found that Aire(+)MHCII(+) type 3 innate lymphoid cells play a critical role in sensing and presenting Candida albicans, and they have a significant impact on the generation of Candida-specific T(H)17 cells.
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 (T(H)17) cell clones. Extrathymic Rorc-Cre-mediated deletion of Aire resulted in impaired generation of Candida-specific T(H)17 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. Abramson and colleagues show that Aire(+)MHCII(+) ILC3s sense, internalize and present Candida albicans and modulate the induction of C. albicans-specific T(H)17 cells.
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