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

Acute Trypanosoma cruzi infection induces an exuberant immune response; however, 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 infection persistence, and increasing the risk of autoimmunity. Cross-reactivity has been demonstrated in CD8 T cells but not in CD4 T cells. Herein, we demonstrate, by cytometry, that CD4+ T cells, carrying the 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, TNF-α, IL-4, and IL-10. In addition, prior oral exposure to OVA altered cytokine production by these transgenic T cells upon infection. We also demonstrate that T. cruzi induces Foxp3 expression in a sizable pool of transgenic T cells.