2026-06-27T12:27:20Zhttps://docta.ucm.es/rest/oai/request

oai:docta.ucm.es:20.500.14352/438792025-02-14T19:19:52Zcom_20.500.14352_14col_20.500.14352_15

00925njm 22002777a 4500 dc Relloso, Miguel author Aragoneses-Fenoll, Laura author Lasarte, Sandra author Bourgeois, Christelle author Romera, Gema author Kuchler, Karl author Corbí, Angel L. author Muñoz-Fernández, María Ángeles author Nombela, César author Rodríguez-Fernández, José L. author Díez-Orejas, Rosalia author 2012-01 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. 1938-3673 10.1189/jlb.1110645 https://hdl.handle.net/20.500.14352/43879 http://www.jleukbio.org Estradiol impairs the Th17 immune response against Candida albicans