Trypanosoma cruzi infection imparts a regulatory program in dendritic cells and T cells via galectin-1-dependent mechanisms

CAROLINA V. PONCINI; JUAN P. CERLIANI; JUAN M. ILARREGUI; ESTELA I. BATALLA

Congreso; IV LASID Meeting-LXIII Argentinean Immunology Society Meeting and II French-Argentinean Immunology Meeting; 2015

Título:Trypanosoma cruzi infection imparts a regulatory program in dendritic cells and T cells via galectin-1-dependent mechanismsAutor/es:PONCINI CV; CERLIANI JP; ILARREGUI JM; BATALLA E; CUCHER M; VAN KOOYK YVETTE; GONZÁLEZ CAPPA SM; RABINOVICH GAReunión:Congreso; IV LASID Meeting-LXIII Argentinean Immunology Society Meeting and II French-Argentinean Immunology Meeting; 2015Resumen:Abstract: Trypanosoma cruzi, the etiological agent of Chagas? disease, is a protozoan parasite that affects ~10 million people in Latin-America. Lately it was increasingly detected in the United States, and European countries due mainly to migratory movements. Infection is generally asymptomatic, however one third of the patients develop dilated cardiomyopathy during chronicity. Galectin-1 (Gal-1), an endogenous glycan-binding protein, is widely distributed at sites of inflammation. In spite of considerable progress regarding its immunoregulatory activity, its role during protozoan-acute infections is uncertain.In this study we show that upon intradermal inoculation of the parasite, Gal-1 functions as a negative regulator to limit host protective immunity. Early during infection, we detected increased Gal-1 expression together with a striking influx of DCs to draining lymph nodes (dLN), followed by the up-regulation of immunomodulatory mediators (p