<em>Trypanosoma cruzi</em> Infection Activates Transgenic DO11.10 CD4+ T Cells

The acute infection with Trypanosoma cruzi induces an exuberant immune response; however, despite this, the host is unable to clear the parasite, and the infection progresses to a chronic phase. T and B cells play a crucial role in controlling infections. Although the parasite presents numerous antigenic determinants capable of activating many T and B cell clones, some antigens trigger a large proportion of CD8 T cells, implying TCR cross-reactivity targeting these determinants. Polyclonal activation may result in an inefficient immune response against the parasite, diverting it toward less critical antigenic determinants, which allows for persistent infection and opens up the possibility of autoimmunity. Cross-reactivity has been demonstrated for CD8 T cells, but not for CD4 T cells. Herein, we demonstrate, using cytometry, that CD4+ T cells expressing high levels of the DO11.10 transgenic TCR, which are responsive to OVA, are activated during T. cruzi acute infection, differentiating into effector memory T cells that produce cytokines such as IFN-γ, TNF-α, and IL-10. Furthermore, prior exposure to OVA via the oral route modified cytokine production of these transgenic T cells upon infection. We also demonstrate that T. cruzi induces the expression of Foxp3 in a sizable pool of transgenic T cells.