Conditional depletion of CD11c-expressing cells greatly compromises innate resistance to skin fungal infection

BECCACECE IGNACIO; ALMEIDA, MARIEL A.; BURSTEIN VL; GUASCONI, LORENA; MENA, CRISTIAN J.; CHIAPELLO LAURA S.

Mar del Plata

Congreso; REUNIÓN ANUAL DE SOCIEDADES DE BIOCIENCIAS. LXX REUNION ANUAL DE LA SOCIEDAD ARGENTINA DE INMUNOLOGÍA-SAI & 3rd FRENCH-ARGENTINE IMMUNOLOGY CONGRESS; 2022

Sociedad Argentina de Inmunología (SAI)

The skin is a physical barrier that protects the body against infectionsowing to several immune cell populations including two major subsets of CD11c+ myeloid cells: Langerhans (LC) and dermal dendriticcells (DC). CARD9 expression (an adaptor molecule downstreampattern recognition receptors) in dendritic cells plays a central role inantifungal immunity, however, the tissue-specific innate immunity remains poorly understood in dermatophytosis. In this study, we aim toinvestigate the in vivo role of skin CD11c+ cells in the susceptibility toexperimental dermatophytic infection. C57BL/6 (WT), CD11c-DTRGFP, Lang-eGFP-DTR or IL-17RA KO mice were epicutaneouslyinfected in the back with Nannizzia gypsea. To deplete CD11c+ cellsor LC, CD11c-DTR-GFP or Lang-eGFP-DTR mice (respectively),received a single dose of diphtheria-toxin (DT, 2 ng/g) 24 h prior toinfection. On 3- and 6-days post-infection (dpi), back skin was treated with Trypsin/EDTA (2 h/37°C) and epidermal cell suspension wasused to perform FACS analysis and to determine cytokines (ELISA),fungal burden and CARD9 gene expression by real time PCR. At anearly time-point of infection (3 dpi), only CD11c+cell-depleted miceshowed a significant increase in fungal burden compared to WT,Lang-eGFP-DTR or IL-17RAKO mice (P