Comment on “Aberrant type 1 immunity drives susceptibility to mucosal fungal infections”-Reference-Cited by-同舟云学术

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

Published:2021-09-17 Issue:6561 Volume:373 Page:
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Kisand Kai¹^ORCID,Meager Anthony²³,Hayday Adrian²⁴³^ORCID,Willcox Nick³⁵

Affiliation:

1. Molecular Pathology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.

2. Regaem Consultants, Whitchurch Gardens, Edgware, Middlesex, UK.

3. Francis Crick Institute, London, UK.

4. Peter Gorer Department of Immunobiology, School of Immunology and Microbial Sciences, King’s College London, London, UK.

5. Department of Clinical Neurosciences, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.

Abstract

Break et al . (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 et al . have focused on late-arising events rather than more common primary causes of CMC.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference15 articles.

1. AIRE-Deficient Patients Harbor Unique High-Affinity Disease-Ameliorating Autoantibodies

2. Chronic mucocutaneous candidiasis in APECED or thymoma patients correlates with autoimmunity to Th17-associated cytokines

3. Anti-Cytokine Autoantibodies Preceding Onset of Autoimmune Polyendocrine Syndrome Type I Features in Early Childhood

4. In vivo analysis of helper T cell responses in patients with autoimmune polyendocrinopathy – candidiasis – ectodermal dystrophy provides evidence in support of an IL-22 defect

5. Mucocutaneous IL-17 immunity in mice and humans: host defense vs. excessive inflammation

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