In a previous study assessing the immune response of CTLA4 to the intracellular protozoan Trypanosoma cruzi, researchers reported a significant increase in CTLA4 expression in the splenic T-cells of infected mice, and the blockade of CTLA4 was shown to increase the production of IFN-γ, TNF-α, and NO, which significantly reduced both parasitemia and mortality in mice infected with the Y strain of T. cruzi and improved host resistance to the Y strain [48]. This evidence concerns the gene CTLA4 and parasitic infectious disease.