Unconventional pro-inflammatory CD4+ T cell response in B cell-deficient mice infected with Trypanosoma cruzi

SERRÁN, MELISA GOROSITO; BOARI, JIMENA TOSELLO; VERNENGO, FACUNDO FIOCCA; BECCARÍA, CRISTIAN G.; RAMELLO, MARÍA C.; BERMEJO, DANIELA A.; COOK, AMELIA G.; VINUESA, CAROLA G.; MONTES, CAROLINA L.; RODRIGUEZ, EVA V. ACOSTA; GRUPPI, ADRIANA

Frontiers in Immunology

Frontiers Media S.A.

Año: 2017 vol. 8

hagas disease, caused by the parasite Trypanosoma cruzi, is endemic in Latin America but has become a global public health concern by migration of infected people. It has been reported that parasite persistence as well as the intensity of the inflammatory immune response are determinants of the clinical manifestations of the disease. Even though inflammation is indispensable for host defense, when deregulated, it can contribute to tissue injury and organ dysfunction. Here, we report the importance of B cells in conditioning T cell response in T. cruzi infection. Mice deficient in mature B cells (muMT mice) infected with T. cruzi exhibited an increase in plasma TNF concentration, TNF-producing CD4+ T cells, and mortality. The increase in TNF-producing CD4+ T cells was accompanied by a reduction in IFNγ+CD4+ T cells and a decrease of the frequency of regulatory Foxp3+, IL-10+, and IL17+CD4+ T cells populations. The CD4+ T cell population activated by T. cruzi infection, in absence