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

BECCACECE IGNACIO; BURSTEIN VERÓNICA; GUASCONI LORENA; MENA CRISTIAN; CERVI LAURA; GRUPPI ADRIANA; CHIAPELLO LAURA

Tucumán

Congreso; LXVII Reunión Científica Anual de la Sociedad Argentina de Inmunología; 2019

Dermatophytosis is a superficial infection caused by filamentous fungi called dermatophytes which damage the skin. Despite this disease has a worldwide prevalence affecting around 25% of the global population, the immunological mechanisms involved in fungal clearance and clinical recovery are still unknown. Previously we have shown that an IL-17-mediated immune response is required to control this infection and not only TCRαβ+ cells but also TCRγδlow cells deal with IL-17 production in the skin in a murine model of dermatophytosis. Little is known about the origin of this TCRαβ+ cells and if they are resident or migrate from lymph nodes (LN) to the site of infection is still under study. The aim of this study was to further characterize this IL-17-producing T cells 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. During the infection, mice were treated with 2µg/g Fingolimod doses (daily intraperitoneal injection) to block the lymphocyte recruitment from LN to skin. 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. FACS analysis revealed that Fingolimod treatment induces a decrease in the number of CD45+ cells, total TCRβ-expressing cells and IL-17 production (P<0.05). However, IL-17-producing TCRβ+ cells are still present and express CD69 suggesting that TCRβ+ skin resident cells are involved in IL-17 production during experimental dermatophytosis.