After Experimental Trypanosoma cruzi Infection, Dying Hepatic CD3(+)TCRαβ(+)B220(+) T Lymphocytes Are Rescued from Death by Peripheral T Cells and Become Activated

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 Trypanosoma cruzi 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.