Comment on "Aberrant type 1 immunity drives susceptibility to mucosal fungal infections"

Break . (Research Articles, 15 January 2021, eaay5731) conclude that T cell overproduction of interferon-γ causes chronic mucocutaneous candidiasis (CMC), a typical early feature of autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy (APECED). This contradicts studies implicating interleu...

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Published in:Science (American Association for the Advancement of Science) 2021-09, Vol.373 (6561), p.eabi6235-eabi6235
Main Authors: Kisand, Kai, Meager, Anthony, Hayday, Adrian, Willcox, Nick
Format: Article
Language:English
Subjects:
Candidiasis
Chronic mucocutaneous candidiasis
Dystrophy
Humans
Interferon
Interleukin 17
Interleukin 22
Lymphocytes
Lymphocytes T
Mucosa
Mucosal immunity
Mucous Membrane
Mycoses
γ-Interferon
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container_title Science (American Association for the Advancement of Science)
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creator Kisand, Kai
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description Break . (Research Articles, 15 January 2021, eaay5731) conclude that T cell overproduction of interferon-γ causes chronic mucocutaneous candidiasis (CMC), a typical early feature of autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy (APECED). This contradicts studies implicating interleukin IL-17 and IL-22 deficiencies as a cause of CMC. We propose that Break . have focused on late-arising events rather than more common primary causes of CMC.
doi_str_mv 10.1126/science.abi6235
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source American Association for the Advancement of Science; Alma/SFX Local Collection
subjects Candidiasis
Chronic mucocutaneous candidiasis
Dystrophy
Humans
Interferon
Interleukin 17
Interleukin 22
Lymphocytes
Lymphocytes T
Mucosa
Mucosal immunity
Mucous Membrane
Mycoses
γ-Interferon
title Comment on "Aberrant type 1 immunity drives susceptibility to mucosal fungal infections"
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