Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 207, Issue 2, Pages 291-297Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20091983
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Funding
- Rockefeller University Center for Clinical and Translational Science [5UL1RR024143-03]
- Institut National de la Sante et de la Recherche Medicale
- University Paris Descartes
- Agence Nationale de la Recherche
- European Union
- March of Dimes
- Dana Foundation
- Addenbrooke's Charitable Trust
- National Institute for Health Research Cambridge Biomedical Research Center
- Howard Hughes Medical Institute
- Hungarian Scientific Research Fund
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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-1 beta, 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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