Extrathymic expression of Aire controls the induction of effective T(H)17 cell-mediated immune response to Candida albicans

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F22%3A00559553" target="_blank" >RIV/68378050:_____/22:00559553 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11310/22:10451180

Výsledek na webu

<a href="https://www.nature.com/articles/s41590-022-01247-6" target="_blank" >https://www.nature.com/articles/s41590-022-01247-6</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/s41590-022-01247-6" target="_blank" >10.1038/s41590-022-01247-6</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Extrathymic expression of Aire controls the induction of effective T(H)17 cell-mediated immune response to Candida albicans

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Extrathymic expression of Aire controls the induction of effective T(H)17 cell-mediated immune response to Candida albicans

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

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OECD FORD obor

30102 - Immunology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2022

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Nature Immunology

ISSN

1529-2908

e-ISSN

1529-2916

Svazek periodika

23

Číslo periodika v rámci svazku

7

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

1098-1108

Kód UT WoS článku

000817057200002

EID výsledku v databázi Scopus

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