期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 41, 期 1, 页码 235-245出版社
WILEY-BLACKWELL PUBLISHING, INC
DOI: 10.1002/eji.200939883
关键词
Autoimmunity; Cytokines; Fungal; T cells
类别
资金
- EURAPS [LSHM-CT-2005, 005223]
- Swedish Medical Research Council
- Thureus foundation
- Italian project PRIN [prot. 2007KLCKP8 004]
- NHMRC [171601, 461204, 257501, 26573, 406700]
Autoimmune polyendocrine syndrome type 1 (APS-1) is a multiorgan autoimmune disease caused by mutations in the autoimmune regulator (AIRE) gene. Chronic mucocutaneous candidiasis, hypoparathyroidism and adrenal failure are hallmarks of the disease. The critical mechanisms causing chronic mucocutaneous candidiasis in APS-1 patients have not been identified although autoantibodies to cytokines are implicated in the pathogenesis. To investigate whether the Th reactivity to Candida albicans (C. albicans) and other stimuli was altered, we isolated PBMC from APS-1 patients and matched healthy controls. The Th17 pathway was upregulated in response to C. albicans in APS-1 patients, whereas the IL-22 secretion was reduced. Autoantibodies against IL-22, IL-17A and IL-17F were detected in sera from APS-1 patients by immunoprecipitation. In addition, Aire-deficient (Aire(0/0)) mice were much more susceptible than Aire(+/+) mice to mucosal candidiasis and C. albicans-induced Th17- and Th1-cell responses were increased in Aire(0/0) mice. Thus an excessive IL-17A reactivity towards C. albicans was observed in APS-1 patients and Aire(0/0) mice.
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