Abstract
Host resistance to Trypanosoma cruzi is dependent on both natural and acquired immune responses. During the acute phase of the infection the presence of IFN-gamma, TNF-alpha, IL-12 and GM-CSF has been closely associated with resistance, whereas TGF-ss and IL-10 have been associated with susceptibility. Several investigators have demonstrated that antibodies are responsible for the survival of susceptible animals in the initial phase of infection and for the maintenance of low levels of parasitemia in the chronic phase. However, how this occurs is not yet understood. Our results and other data in the literature support the hypothesis that the protective role of antibodies in the acute phase of infection is dependent mostly on their ability to induce removal of bloodstream trypomastigotes from the circulation in addition to other concomitant cell-mediated events.
Highlights
Trypanosoma cruzi, the causative agent of Chagas disease, is a protozoan parasite that affects millions of people in Latin America
During the acute phase of the infection the presence of IFN-g, TNF-a, IL-12 and GM-CSF has been closely associated with resistance, whereas TGF-ß and IL-10 have been associated with susceptibility
IFN-g, TNF-a, IL-12 [1] and GM-CSF [2] seem to be the cytokines most closely associated with the control of the parasitemia and mortality of resistant mice in the acute phase of the disease
Summary
Trypanosoma cruzi, the causative agent of Chagas disease, is a protozoan parasite that affects millions of people in Latin America. Our results and other data in the literature support the hypothesis that the protective role of antibodies in the acute phase of infection is dependent mostly on their ability to induce removal of bloodstream trypomastigotes from the circulation in addition to other concomitant cell-mediated events.
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Schedule a callMore From: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
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