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Glycans of Trypanosoma cruzi virulence factors are effective targets for vaccine development

Trypanosoma cruzi causes Chagas disease (CD), which affects millions of people. There is no human vaccine despite numerous experimental studies based on T‐cell epitopes. In contrast, B‐cell epitopes remain poorly explored, despite the fact that very high levels of protective anti‐α‐Gal Abs elicited against highly abundant α‐Gal epitopes on the parasite surface are ubiquitous in CD patients. We hypothesize that terminal α‐Gal‐containing epitopes are potential vaccine targets. Here, we evaluate the Galα1,3LacNAc‐BSA in the α1,3‐galactosyltransferase‐KO (αGalT‐KO) mouse model, which closely mimics the human humoral immune response against T. cruzi. Following immunization, αGalT‐KO mice showed high titers of protective anti‐α‐Gal Abs, very low parasitemia, and high levels of proinflammatory cytokines. All immunized animals survived up to one year (experiment endpoint) following parasite challenges. Histological and qRT‐PCR analyses of the heart of protected animals indicated extremely low parasite levels. Depletion of CD4+ and/or CD8+ T cells before or after immunization resulted in much lower survival rates, corroborating the key role of T cells in controlling disease progression. In sum, our data show that protective anti‐α‐Gal Abs and proinflammatory immune responses can effectively control experimental CD.