Protection against mucocutaneous candidiasis depends on the T helper (Th)17 
pathway, as gene defects affecting its integrity result in inability to clear 
Candida albicans infection on body surfaces. Moreover, autoantibodies 
neutralizing Th17 cytokines have been related to chronic candidiasis in a rare 
inherited disorder called autoimmune polyendocriopathy candidiasis ectodermal 
dystrophy (APECED) caused by mutations in autoimmune regulator (AIRE) gene. 
However, the direct pathogenicity of these autoantibodies has not yet been 
addressed. Here we show that the level of anti-IL17A autoantibodies that develop 
in aged Aire-deficient mice is not sufficient for conferring susceptibility to 
oropharyngeal candidiasis. However, patient-derived monoclonal antibodies that 
cross-react with murine IL-22 increase the fungal burden on C. albicans infected 
mucosa. Nevertheless, the lack of macroscopically evident infectious pathology 
on the oral mucosa of infected mice suggests that additional susceptibility 
factors are needed to precipitate a clinical disease.