Characterization of skin IL-17-producing T cell populations in experimental dermatomycosis

BECCACECE I; BURSTEIN VL; GUASCONI L; MENA C; CERVI L; GRUPPI A; CHIAPELLO LS

Congreso; LXVII Reunión anual de la Sociedad Argentina de Inmunología.; 2019

Despite skin fungal infections affect around 25% of the global population, the tissue-specific immunity against dermatophytes is poorly understood. Previously, we have demonstrated that IL-17-mediated immune response controls fungal proliferation in the skin during the experimental infection of C57BL/6 mice with Microsporum spp. Furthermore, epidermal TCRαβ+ and TCRγδ+ cells were the main producers of IL-17A after infection, but if these T cell populations are skin resident or migrate from lymph nodes (LN) to the site of infection is still unknown.The aim of this study was to further characterize IL-17-producing T cells populations in the skin, emphasizing on TCRβ-expressing T cells. In order to this, IL-17A-GFP reporter mice were epicutaneously infected in their back with a Microsporum gypseum hyphae suspension or treated with saline (uninfected controls). In parallel, infected or control mice were treated with 2μg/g fingolimod doses (daily intraperitoneal injection) to block the lymphocyte recruitment from LN to skin (CICUAL: Res. Nº 739/2018). After 8 days post-infection mice were euthanized and epidermal cells were obtained and studied by FACS using anti-CD45, anti-TCRβ, anti-TCRγδ, and anti-CD69 antibodies.Flow cytometry analysis revealed that fingolimod treatment reduces the number of CD45+ epidermal cells, and IL-17-producing TCRβ-expressing cells after infection (P<0.05). However, despite fingolimod-treatment, infected mice still harbored a significant population of IL-17-producing TCRβ+ cells in the skin, with high levels of CD69 expression.These results strongly suggest that a population of skin resident TCRβ+ lymphocytes is involved in IL-17 -mediated antifungal immunity during experimental dermatomycosis.