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Trypanosoma cruzi  infection is characterized by chronic parasitism of non-lymphoid tissues and is rarely eliminated despite potent adaptive immune responses. This failure to cure has frequently been attributed to a loss or impairment of anti- T .  cruzi  T cell responses over time, analogous to the T cell dysfunction described for other persistent infections. In this study, we have evaluated the role of CD8 +  T cells during chronic  T .  cruzi  infection (&gt;100 dpi), with a focus on sites of pathogen persistence. Consistent with repetitive antigen exposure during chronic infection, parasite-specific CD8 +  T cells from multiple organs expressed high levels of KLRG1, but exhibit a preferential accumulation of CD69 +  cells in skeletal muscle, indicating recent antigen encounter in a niche for  T .  cruzi  persistence. A significant proportion of CD8 +  T cells in the muscle also produced IFNγ, TNFα and granzyme B  in situ , an indication of their detection of and functional response to  T .  cruzi in vivo . CD8 +  T cell function was crucial for the control of parasite burden during chronic infection as exacerbation of parasite load was observed upon depletion of this population. Attempts to improve T cell function by blocking PD-1 or IL-10, potential negative regulators of T cells, failed to increase IFNγ and TNFα production or to enhance  T .  cruzi  clearance. These results highlight the capacity of the CD8 +  T cell population to retain essential  in vivo  function despite chronic antigen stimulation and support a model in which CD8 +  T cell dysfunction plays a negligible role in the ability of  Trypanosoma cruzi  to persist in mice.

Highly competent, non-exhausted CD8+ T cells continue to tightly control pathogen load throughout chronic Trypanosoma cruzi infection