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      Chronic mucocutaneous candidiasis in humans with inborn errors of interleukin-17 immunity.

      Science (New York, N.Y.)

      Candida albicans, immunology, Th17 Cells, genetics, Signal Transduction, Receptors, Interleukin-17, Pedigree, Mutation, Molecular Sequence Data, Male, Interleukin-17, Humans, Genes, Recessive, Genes, Dominant, Female, Child, Preschool, Child, Candidiasis, Chronic Mucocutaneous

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          Abstract

          Chronic mucocutaneous candidiasis disease (CMCD) is characterized by recurrent or persistent infections of the skin, nails, and oral and genital mucosae caused by Candida albicans and, to a lesser extent, Staphylococcus aureus, in patients with no other infectious or autoimmune manifestations. We report two genetic etiologies of CMCD: autosomal recessive deficiency in the cytokine receptor, interleukin-17 receptor A (IL-17RA), and autosomal dominant deficiency of the cytokine interleukin-17F (IL-17F). IL-17RA deficiency is complete, abolishing cellular responses to IL-17A and IL-17F homo- and heterodimers. By contrast, IL-17F deficiency is partial, with mutant IL-17F-containing homo- and heterodimers displaying impaired, but not abolished, activity. These experiments of nature indicate that human IL-17A and IL-17F are essential for mucocutaneous immunity against C. albicans, but otherwise largely redundant.

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          Author and article information

          Journal
          10.1126/science.1200439
          21350122
          3070042

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