backend=biber, style=alphabetic, sorting=ynt ]biblatex Introduction: Trypanosoma cruzi infection, which causes Chagas’ disease, induces an immune response in the host whose efficiency is important for the infection to persist or be eliminated. Alcohol consumption produces a great impact on the immune system, inducing alterations in the determination of T lymphocyte effector function, directing the profile of these cells to tolerance or inflammation. Our study aimed to evaluate, in C57BL/6 mice, the cytokine production in splenic leukocytes from T. cruzi infected and treated (EtOH) for 15 days and controls. Methods: Twenty-four mice were randomized into four groups, with 12 animals each: (1) Non-Infected Control (NI), (2) Control Infected (CI), (3) Experimental Non-Infected (EtOH _-NI), and (4) Experimental Infected (EtOH _-I). Results: Ethanol-pre-exposed infected mice exhibited elevated parasitemia during the patent period compared to controls. Adaptive immunity was characterized by increased IL-4, IL-10, and IFN-γ production by CD8+ T lymphocytes, while innate immunity showed reduced cytokine production, particularly in NK cells and macrophages. Ethanol amplified IL-10 and IFN-γ responses in macrophages yet suppressed TNF-α production in dendritic cells and macrophages during infection. Conclusion: These findings suggest ethanol modulates the immune response by enhancing adaptive immunity while impairing innate mechanisms, contributing to altered host-pathogen dynamics in T. cruzi infection.