Role of the signaling of IL-17A on the autophagy process during human tuberculosis

TATEOSIAN NANCY L; ROLANDELLI AGUSTIN; LEVI ALBERTO; COLOMBO MARISA I; AMIANO NICOLAS O; CASTELLO FLORENCIA A; PALMERO DOMINGO J; PELLEGRINI JOAQUIN M; MORELLI MARIA PAULA; CASCO NICOLAS; GARCÍA VERÓNICA E

Mar del Plata

Congreso; LXI Reunión Científica Anual de la Sociedad Argentina de Investigaciones Clinicas (SAIC), LXIV Reunión Anual de la Sociedad Argentina de Inmunología (SAI) y XLVIII Reunión Anual de la Sociedad Argentina de Farmacología Experimental (SAFE); 2016

An appropriate immune response against Mycobacterium tuberculosis (Mtb) requires Th1 cytokine responses but IFN-gamma alone is not enough to the complete bacterial eradication. Actually, Th17 cells have been associated with Mtb infection. Autophagy is an immune effector mechanism against intracellular pathogens, positively modulated by Th1 cytokines, and negatively regulated by Th2 cytokines. However, the role of other cytokines on autophagy in tuberculosis patients (TB) remains unknown. Here we study the role of IL-17A on autophagy during active human TB. Monocytes (Mo) from TB patients and healthy donors (HD) were infected with Mtb H37Rv pathogenic strain and cultured ± IL-17A (10ng/ml, 24h). Then autophagy levels were analyzed by Flow cytometry and Immunofluorescence Microscopy against LC3-IIB. We observe that IL-17A increased autophagy against Mtb-H37Rv in Mo from HD and TB patients that display strong immunity against Mtb (HR TB; p