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The contribution of T-cell subpopulations to immunopathology in murine Trypanosoma cruzi infection was studied by using in situ localization of lymphocytes and in vivo depletion of T-lymphocyte populations. CD8+ T cells were the major lymphocyte population in the inflamed hearts of C3H/HeSnJ mice infected with the Sylvio X10/4 clone of T. cruzi at all time points of the acute and chronic phases of the infection examined. Depletion of CD8+ and/or CD4+ T cells beginning on day 20 of the infection resulted in a moderate decrease in the inflammation and an increase in parasite burden in the hearts of mice at day 30 of infection. Longer-term depletion, beginning at day 20 and extending as long as 200 days of infection, resulted in an increased inflammatory response in the heart. A large proportion of the inflammatory cells in the hearts of anti-CD8- or anti-CD4- and anti-CD8-treated mice were Thy1+ and CD4- CD8-. At 200 days of infection, the increased inflammation was accompanied by an increase in the parasite load in the heart. These results show that T-cell subset depletion does not prevent the inflammatory response associated with acute and chronic T. cruzi infection. The increased parasite load in T-cell-depleted mice also demonstrates the participation of these T-cell subsets in regulation of parasite load throughout the course of the infection. The increased inflammatory response despite T-cell depletion and in association with increased numbers of tissue parasites suggests that intracellular parasites are a driving force behind the inflammatory response in chronic murine T. cruzi infection.

Depletion of T-cell subpopulations results in exacerbation of myocarditis and parasitism in experimental Chagas' disease