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Front. Immunol. | doi: 10.3389/fimmu.2018.02570

Chronic Mucocutaneous Candidiasis in Autoimmune Polyendocrine Syndrome Type 1

 Boualem Sendid1*,  linda Humbert2,  marjorie Cornu1, Emmanuelle Proust-Lemoine3,  Jagadeesh BAYRY4, Jean Louis Wemeau5 and Marie Christine Vantyghem6
  • 1INSERM U995 Centre international de recherche sur l'inflammation de Lille, France
  • 2Centre Hospitalier Regional et Universitaire de Lille, France
  • 3Clinique Aguiléra, France
  • 4INSERM U1138 Centre de Recherche des Cordeliers, France
  • 5Département de Endocrinologie Diabétologie Métabolismes, Centre Hospitalier Regional et Universitaire de Lille, France
  • 6INSERM U1190 Recherche Translationnelle sur le Diabète, France

Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) is an autosomal recessive disease caused by mutations in the autoimmune regulator (AIRE) gene, characterized by the clinical triad of chronic mucocutaneous candidiasis (CMC), hypoparathyroidism, and adrenal insufficiency. CMC can be complicated by systemic candidiasis or oral squamous cell carcinoma (SCC), and may lead to death. The role of chronic Candida infection in the etiopathogenesis of oral SCC is unclear. Long-term use of fluconazole has led to the emergence of Candida albicans strains with decreased susceptibility to azoles. CMC is associated with an impaired Th17 cell response; however, it remains unclear whether decreased serum IL-17 and IL-22 levels are related to a defect in cytokine production or to neutralizing autoantibodies resulting from mutations in the AIRE gene.

Keywords: autoimmune polyendocrinopathycandidiasisectodermaldystrophy (APECED), Chronic mucocutaneous candidiasis (CMC), autoimmune regulator (AIRE) gene, IL-17, IL-22

Received: 24 Aug 2018; Accepted: 18 Oct 2018.

Edited by:

Sudhanshu Shekhar, University of Oslo, Norway

Reviewed by:

Jeanette Wagener, University of Aberdeen, United Kingdom
Desa Lilic, Newcastle University, United Kingdom
Marc Swidergall, UCLA Department of Medicine, United States  

Copyright: © 2018 Sendid, Humbert, Cornu, Proust-Lemoine, BAYRY, Wemeau and Vantyghem. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Boualem Sendid, INSERM U995 Centre international de recherche sur l'inflammation de Lille, Lille, France, boualem.sendid@univ-lille.fr