Interleukin 17-producing epidermal cell subsets in experimental Microsporum canis dermatophytosis.

BECCACE, IGNACIO; BURSTEIN, VERONICA; GUASCONI, LORENA; MENA, CRISTIAN; GRUPPI, ADRIANA; THEUMER, MARTIN; CERVI, LAURA; CHIAPELLO, LAURA

Buenos Aires

Congreso; Reunión Conjunta de Sociedades de Biociencias 2017; 2017

SAI - SAIC - SAP - SAIB etc

(826) INTERLEUKIN 17-PRODUCING EPIDERMAL CELLSUBSETS IN EXPERIMENTAL MICROSPORUM CANISDERMATOPHYTOSISIgnacio Beccacece (1), Verónica Burstein (1), LorenaGuasconi (1), Cristian Mena (1), Adriana Gruppi (1), MartinTheumer (1), Laura Cervi (1), Laura Chiapello (1)(1) Departamento de Bioquímica Clínica. Facultad de CienciasQuímicas. UNC. CIBICI-CONICET.Microsporum canis is a dermatophyte fungus that causes highlyprevalent skin infections in immunocompetent children. We previouslydemonstrated that a Th17 response is induced after epicutaneousinfection of C57BL/6 mice with M. canis and that IL-17-mediatedimmunity prevents fungal proliferation in skin. However, themechanisms of dermatophyte recognition and skin cell populationsinvolved in IL-17-driven host defense remain unknown.The aim of this study was to determine skin cell sources of IL-17Aand the role of TLR-2 and Dectin-1 receptors in the protective immunityagainst M. canis infection.Wild type (WT), IL-17GFP reporter, IL-17RAKO, TLR-2KO andDectin-1KO C57BL/6 mice were epicutaneously infected with M.canis hyphae or treated with saline. After 8 days of infection, skinfungal burden was determined and IL-17A-producing epidermal cellpopulations were evaluated by FACS with anti-CD45, CD11b, Ly6G,TCRb, TCRγd, CD3, CD4 or CD8 antibodies. Cytokine productionby epidermal sheets explants was quantified in supernatants (ELISA)after 48h of culture with or without M. canis.We observed that, in M canis-infected IL-17GFP reporter mice,CD45+TCRb+ and TCRγd+ epidermal cells were the main IL-17Aproducing-cells. No IL-17 expression was observed in keratinocytes,neutrophils or macrophages. In addition, after culture with epidermalsheets explants, M. canis significantly increased IL-6 and IL-1b (IL-17-type response cytokines) respect to controls in medium alone.Furthermore, infected IL-17RA KO mice showed a significant increasein fungal burden respect to WT mice (38200 ± 13980 vs 867 ±392 CFU/g, p < 0.05). TLR-2 or dectin-1 deficient mice showed asimilar fungal burden and IL-17-producing T cell frequency comparedto infected WT mice.This study is the first characterization of skin IL-17-producing cellsin dermatophytosis and it strongly suggests that TLR-2 or Dectin-1receptors are not involved in the IL-17-driven host protection againstM. canis.Keywords: Skin immunity, fungi, IL-17, Tgd