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Rockefeller University Press, Journal of Experimental Medicine, 2(207), p. 291-297, 2010

DOI: 10.1084/jem.20091983

Elsevier, Year Book of Medicine, (2011), p. 31-32

DOI: 10.1016/j.ymed.2011.09.007

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Autoantibodies against IL-17A, IL-17F, and IL-22 in patients with chronic mucocutaneous candidiasis and autoimmune polyendocrine syndrome type I

Journal article published in 2010 by Anne Puel, Rainer Döffinger, Angels Natividad, Maya Chrabieh ORCID, Gabriela Barcenas-Morales, Capucine Picard ORCID, Aurélie Cobat, Marie Ouachée-Chardin, Antoine Toulon, Jacinta Bustamante, Saleh Al-Muhsen, Mohammed Al-Owain, Peter D. Arkwright, Colm Costigan, Vivienne McConnell and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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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.