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The unusual phenotype of CD3⁺ T lymphocyte expressing B220, a marker originally attributed to B lymphocytes, was first observed in the liver of Fas/Fas-L-deficient mice as a marker of apoptotic T lymphocytes. However, other CD3⁺B220⁺ T lymphocyte populations were later described in the periphery as functional cytotoxic or regulatory cells, for example. Then, in this work, we studied whether hepatic CD3⁺B220⁺ T lymphocytes could play a role in experimental <i>Trypanosoma cruzi</i> infection. In control and infected mice, we observed two subpopulations that could be discerned based on CD117 expression, which were conventional apoptotic CD3⁺B220⁺(CD117⁻) and thymus-independent CD3⁺B220⁺CD117⁺ T lymphocytes. Regardless of CD117 expression, most B220⁺ T lymphocytes were 7AAD⁺, confirming this molecule as a marker of dying T cells. However, after infection, we found that around 15% of the CD3⁺B220⁺CD117⁺ hepatic population became B220 and 7AAD negative, turned into CD90.2⁺, and upregulated the expression of CD44, CD49d, and CD11a, a phenotype consistent with activated T lymphocytes. Moreover, we observed that the hepatic CD3⁺B220⁺CD117⁺ population was rescued from death by previously activated peripheral T lymphocytes. Our results extend the comprehension of the hepatic CD3⁺B220⁺ T lymphocyte subpopulations and illustrate the complex interactions that occur in the liver.