Cross-presentation of antigens from Trypanosoma cruzi

LUCIA BISCARI; PAULA CAMBRONERA; MARÍA CARMEN MAZA MORENO; NABILA COCORDANO; CECILIA FARRÉ; NURIA GIRONÈS PUJOL; ANA ROSA PÉREZ; ANDRÉS ALLOATTI

Tucumán

Congreso; LXVII Reunión científica anual de la Sociedad Argentina de Inmunología; 2019

Sociedad Argentina de Inmunología

Abstract71. CROSS-PRESENTATION OF ANTIGENS FROM Trypanosoma cruziBiscari L1, Cambronera P1, Maza Moreno MC2, Cocordano N1, Farré C1, Girones Pujol N2, PérezAR1, Alloatti A1.1Instituto de Inmunología Clínica y Experimental De Rosario, CONICET-UNR. 2Centro de BiologíaMolecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma deMadrid, Cantoblanco, Madrid, Spain.Chagas? disease, whose etiological agent is the parasite Trypanosoma cruzi, affects 8 millionpeople worldwide, and cause 15.000 deaths per year. Endemic in Latin America, migration fromdeveloping to developed countries also spread the infection to the US and Europe. Currenttreatments are difficult to administer and present high toxicity. Also, there are no vaccines toprevent or fight the disease. Hence, elucidating the ways by which the anti-parasite immuneresponse is generated will serve to develop novel tools favoring a better infection control. It hasbeen shown that CD8+ T cell responses are of utmost relevance for controlling the infection, butlittle is known about how these cytotoxic responses are primed.In this work, we use a recently developed mouse line, Sec22bKO, deficient in antigen crosspresentation(but not the classical antigen presentation pathways), to analyze whether suchmechanism is of relevance to mount anti-parasite CD8+ T cell responses. We infected Sec22bWTand Sec22bKO mice with tripomastigotes of T. cruzi (strain Y). We analyzed CD8+ T cellresponses (global and specific), parasitemia, corporal weight and survival.Sec22bKO mice primed deficient CD8+ T cell responses, either specific for the parasite or general.Additionally, the effector T cell development was affected in Sec22bKO mice. As a consequence,parasitemia was higher and earlier in Sec22bKO, and these mice also lost around 20% of theirweight to finally die 30 days after infection, whereas Sec22bWT survived.Hence, cross-presentation is a relevant mechanism contributing to elicit immune responses thatwill help controlling T. cruzi infection.