Oxidative stress induced by glycolisis drives the crosstalk between monocytes and T cells in human Chagas disease

AOKI, MARIA PILAR; ANGEL RAMÓN MINGUEZ; QUEBRADA PALACIO LUZ PIEDAD ; MORELLI LAURA; MARTINO ADAMI PAMELA; SANMARCO, LILIANA MARIA; POSTAN MIRIAM; LAURA MARINA VISCONTI; EBERHARDT, NATALIA

Cancún

Congreso; XII Congress of the Latin American Association of Immunology - ALAI XXIII Congress of the Mexican Society of Immunology - SMI; 2018

Latin American Association of Immunology - ALAI - Mexican Society of Immunology - SMI

AbstractChagas disease is caused by Trypanosoma cruzi infection and constitutes a major public health problem in Latin America due to its prevalence, morbidity and mortality. The host?s ability to control infection is substantial, but not fully effective, since most infected individuals tightly limit parasite load but fail to completely clear the infection due to diverse and fascinating immune evasion processes. Although nitric oxide (NO) is key as anti-trypanosomal agent, persistent levels of NO are also involved in the induction of lymphocyte unresponsiveness, since it triggers the nitration of T-cell surface proteins. In this sense, we have recently reported that circulating leukocytes from Chagas disease patients exhibit increased NO production concomitant with augmented nitration of CD8+ T cells and impaired cytotoxic functions. In addition, a substantial contraction of T cell compartment at the expense of CD8+ T cells is observed in peripheral blood from Chagas disease patients. Taking into account that monocytes (Mo) are one of the main sources of NO; our aim was to elucidate the crosstalk between Mo and T cells in human Chagas disease, characterizing the frequency of Mo subsets and their effector functions, and determining the mechanism that drives Mo-T cell interaction. Similar to bacterial and viral infections, the proportion of circulating classical Mo decreased (p