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The opportunistic fungal pathogen  Candida albicans  frequently causes diseases such as o ropharyngeal candidiasis  (OPC) in immunocompromised individuals. Although it is well appreciated that the cytokine IL-17 is crucial for protective immunity against OPC, the cellular source and the regulation of this cytokine during infection are still a matter of debate. Here, we directly visualized IL-17 production in the tongue of experimentally infected mice, thereby demonstrating that this key cytokine is expressed by three complementary subsets of CD90 +  leukocytes: RAG-dependent αβ and γδ T cells, as well as RAG-independent ILCs. To determine the regulation of IL-17 production at the onset of OPC, we investigated in detail the myeloid compartment of the tongue and found a heterogeneous and dynamic mononuclear phagocyte (MNP) network in the infected tongue that consists of Zbtb46 - Langerin -  macrophages, Zbtb46 + Langerin +  dendritic cells (DCs) and Ly6C +  inflammatory monocytes. Of those, the Langerin +  DC population stands out by its unique capacity to co-produce the cytokines IL-1β, IL-6 and IL-23, all of which promote IL-17 induction in response to  C .  albicans  in the oral mucosa. The critical role of Langerin +  DCs for the innate IL-17 response was confirmed by depletion of this cellular subset  in vivo , which compromised IL-17 induction during OPC. In conclusion, our work revealed key regulatory factors and their cellular sources of innate IL-17-dependent antifungal immunity in the oral mucosa.

Langerin+ DCs regulate innate IL-17 production in the oral mucosa during Candida albicans-mediated infection