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

The acute Trypanosoma cruzi infection 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 constitutes a myriad of 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 to less critical antigenic determinants, allowing for infection persistence, and opening up the possibility of autoimmunity. Cross-reactivity is being demonstrated for CD8 T cells, but not for CD4 T cells. Herein, we demonstrate, by cytometry, that CD4+ T cells, carrying high levels of DO11.10 transgenic TCR, which are responsive to OVA, are activated during the T. cruzi acute infection, becoming effector memory T cells that produce cytokines such as IFN-γ and TNF-α, and 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.