Resumen:
Microsporum canis is a dermatophyte fungus highly prevalentin immunocompetent children that causes superfcial infections.HoYever, invasion beyond epidermis has also been reported.The in vivo role of +L and Langerhans cells LC during dermatophytosis is currently unMnoYn. 1bjective To determine theimpact of +L signaling in experimental dermatophytosis in miceand the role of LC in establishing sMin antifungal immunity. 9ildtype 9T, +L4A-1, +LA/F-1 or LangE)F2&T4 C$L/mice Yere epicutaneously infected Yith M. canis. For LC depletion, diphtheria toxin Yas injected days before infection. 1n, and days postinfection dpi histopathological analysis,sMin fungal burden H2LC ergosterol quantifcation and fungaldissemination Yere determined. C&b Ly) , T cells populations and cytoMine production Yere analyzed EL+SA, FACS inepidermis or sMindraining lymph node sdL0 cells. CytoMinesYere also measured in epidermal sheet explants incubated YithM. canis. 9T mice resolved infection by dpi shoYing featuresof human dermatophytosis. The response Yas mainly characterized by signifcant neutrophilic sMin infltrate and +LproducingCD4 T cells in sdL0s by dpi. M. canis hyphae stimulated +LA/F, +L, +L, +L and +L production by epidermal cellsand purifed LC promoted only +LA/F production by allogeneiclymphocytes. +L defcient mice resolved infection similar to9T, but shoYed higher sMin inflammation and fungal burden anda shift to +F0º production in sdL0s, compared to 9T mice. Invivo +F0º blocMing partially inhibited the exacerbated cutaneousinflammation and LC depletion in LangE)F2&T4 mice shoYedsignifcant decrease in M. canis specifc +Lproducing C& Tcells. Langerhans cells induce Th antifungal immunity. +Lsignaling protects against M. canis infection and the exacerbatedTh inflammation, but is not involved in 2/0 recruitment to sMinor in control of extracutaneous fungal dissemination.