Autoantibodies Against IL-17A, IL-17F, and IL-22 in Patients with Chronic Mucocutaneous Candidiasis and Autoimmune Polyendocrine Syndrome Type I

Overview

Journal J Exp Med

Specialties Allergy & Immunology
General Medicine

Date 2010 Feb 4

PMID 20123958

Citations 330

Authors

Anne Puel

Rainer Doffinger

Angels Natividad

Maya Chrabieh

Gabriela Barcenas-Morales

Capucine Picard

Aurelie Cobat

Marie Ouachee-Chardin

Antoine Toulon

Jacinta Bustamante

Saleh Al-Muhsen

Mohammed Al-Owain

Peter D Arkwright

Colm Costigan

Vivienne McConnell

Andrew J Cant

Mario Abinun

Michel Polak

Pierre-Francois Bougneres

Dinakantha Kumararatne

Laszlo Marodi

Amit Nahum

Chaim Roifman

Stephane Blanche

Alain Fischer

Christine Bodemer

Laurent Abel

Desa Lilic

Jean-Laurent Casanova

Affiliations

Soon will be listed here.

Abstract

Most patients with autoimmune polyendocrine syndrome type I (APS-I) display chronic mucocutaneous candidiasis (CMC). We hypothesized that this CMC might result from autoimmunity to interleukin (IL)-17 cytokines. We found high titers of autoantibodies (auto-Abs) against IL-17A, IL-17F, and/or IL-22 in the sera of all 33 patients tested, as detected by multiplex particle-based flow cytometry. The auto-Abs against IL-17A, IL-17F, and IL-22 were specific in the five patients tested, as shown by Western blotting. The auto-Abs against IL-17A were neutralizing in the only patient tested, as shown by bioassays of IL-17A activity. None of the 37 healthy controls and none of the 103 patients with other autoimmune disorders tested had such auto-Abs. None of the patients with APS-I had auto-Abs against cytokines previously shown to cause other well-defined clinical syndromes in other patients (IL-6, interferon [IFN]-gamma, or granulocyte/macrophage colony-stimulating factor) or against other cytokines (IL-1beta, IL-10, IL-12, IL-18, IL-21, IL-23, IL-26, IFN-beta, tumor necrosis factor [alpha], or transforming growth factor beta). These findings suggest that auto-Abs against IL-17A, IL-17F, and IL-22 may cause CMC in patients with APS-I.

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