Chagas disease caused by Trypanosoma cruzi affects approximately 7 million people in Latin America. Furthermore, blood transfusion and organ transplantation are health problems in countries receiving migrants from endemic areas. Cardiac pathology is the most serious and characteristic manifestation and a future incidence of between 6,000 and 30,000 cases of Chagas cardiomyopathy is estimated in Spain. Chagas disease is a neglected tropical disease for which there is no effective treatment for the chronic phase of the disease or reliable prognostic markers. Our research aims to understand how immunopathology is generated focusing on the immunoregulatory mechanisms mediated by myeloid suppressor cells (MDSCs). MDSCs are immature myeloid cells that expand in tumor processes, trauma, and infections. They are characterized by the expression of inducible nitric oxide synthase (iNOS) and arginase 1 (ARG1) that use the substrate L-arginine for the production of inflammatory mediators such as nitric oxide (NO) with antimicrobial effect, and with proliferative and tissue repairing effects, respectively. In this context, we have observed that infection by the parasite causes the expansion of MDSCs and a drastic reduction in the levels of L-arginine, which inhibits the proliferation of T cells and RNS, including nitric oxide (NO) produced by the iNOS. Supplementation with L-arginine in infected mice produced a decrease in mortality and an improvement in the clinical score of the mice and could be used in combination therapy.