Estradiol impairs the Th17 immune response against Candida albicans

In vivo and ex vivo E2‐treated DCs have diminished ability to trigger the Th17 immune response against C. albicans antigens. Candida albicans is a commensal opportunistic pathogen that is also a member of gastrointestinal and reproductive tract microbiota. Exogenous factors, such as oral contraceptives, hormone replacement therapy, and estradiol, may affect susceptibility to Candida infection, although the mechanisms involved in this process have not been elucidated. We used a systemic candidiasis model to investigate how estradiol confers susceptibility to infection. We report that estradiol increases mouse susceptibility to systemic candidiasis, as in vivo and ex vivo estradiol‐treated DCs were less efficient at up‐regulating antigen‐presenting machinery, pathogen killing, migration, IL‐23 production, and triggering of the Th17 immune response. Based on these results, we propose that estradiol impairs DC function, thus explaining the increased susceptibility to infection during estrus.