Artículos de revistas
Interleukin-17-induced Protein Lipocalin 2 Is Dispensable For Immunity To Oral Candidiasis
Registro en:
Infection And Immunity. , v. 82, n. 3, p. 1030 - 1035, 2014.
199567
10.1128/IAI.01389-13
2-s2.0-84894285479
Autor
Ferreira M.C.
Whibley N.
Mamo A.J.
Siebenlist U.
Chan Y.R.
Gaffen S.L.
Institución
Resumen
Oropharyngeal candidiasis (OPC; thrush) is an opportunistic fungal infection caused by the commensal microbe Candida albicans. Immunity to OPC is strongly dependent on CD4+ T cells, particularly those of the Th17 subset. Interleukin-17 (IL-17) deficiency in mice or humans leads to chronic mucocutaneous candidiasis, but the specific downstream mechanisms of IL-17- mediated host defense remain unclear. Lipocalin 2 (Lcn2; 24p3; neutrophil gelatinase-associated lipocalin [NGAL]) is an antimicrobial host defense factor produced in response to inflammatory cytokines, particularly IL-17. Lcn2 plays a key role in preventing iron acquisition by bacteria that use catecholate-type siderophores, and lipocalin 2-/- mice are highly susceptible to infection by Escherichia coli and Klebsiella pneumoniae. The role of Lcn2 in mediating immunity to fungi is poorly defined. Accordingly, in this study, we evaluated the role of Lcn2 in immunity to oral infection with C. albicans. 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