Abstract
Trypanosoma cruzi interacts with the different arms of the innate and adaptive host's immune response in a very complex and flowery manner. The history of host-parasite co-evolution has provided this protozoan with means of resisting, escaping or subverting the mechanisms of immunity and establishing a chronic infection. Despite many decades of research on the subject, the infection remains incurable, and the factors that steer chronic Chagas disease from an asymptomatic state to clinical onset are still unclear. As the relationship between T. cruzi and the host immune system is intricate, so is the amount and diversity of scientific knowledge on the matter. Many of the mechanisms of immunity are fairly well understood, but unveiling the factors that lead each of these to success or failure, within the coordinated response as a whole, requires further research. The intention behind this Review is to compile the available information on the different aspects of the immune response, with an emphasis on those phenomena that have been studied and confirmed in the human host. For ease of comprehension, it has been subdivided in sections that cover the main humoral and cell-mediated components involved therein. However, we also intend to underline that these elements are not independent, but function intimately and concertedly. Here, we summarize years of investigation carried out to unravel the puzzling interplay between the host and the parasite.
Highlights
More than a century after its discovery, Chagas disease continues to be one of the main public health problems in South and Central America, with approximate numbers of 6–7 million people infected in the world, 100 million at risk of infection, 56 thousand new cases per year and 12 thousand deaths per year [1, 2]
Experiments with mouse bone marrow-derived dendritic cells (DCs) showed that inhibitory receptor SIGLEC-E is activated by the sialylated ligands on the parasite surface, downregulating IL-12 secretion and upregulating that of IL-10 [62], and may be involved in immunomodulatory mechanisms associated to T. cruzi infection
Across several decades of research, a remarkable volume of information regarding the immune response to T. cruzi infection and its role in protection, chronicity, inflammation and pathology has accumulated
Summary
More than a century after its discovery, Chagas disease continues to be one of the main public health problems in South and Central America, with approximate numbers of 6–7 million people infected in the world, 100 million at risk of infection, 56 thousand new cases per year and 12 thousand deaths per year [1, 2]. Experiments with mouse bone marrow-derived DCs showed that inhibitory receptor SIGLEC-E is activated by the sialylated ligands on the parasite surface, downregulating IL-12 secretion and upregulating that of IL-10 [62], and may be involved in immunomodulatory mechanisms associated to T. cruzi infection This is in agreement with results by Ersching et al who used a murine model to demonstrate that DCs that have been exposed to T. cruzi induce regulatory T (Treg) cells with an enhanced suppressor capacity on CD8+ T cells [63]. The observation of a decrease in the infective capacity of the parasite on cultured mouse fibroblasts in the presence of total spleen cells, that is reverted when NK cells are depleted, has been pointed out as evidence for a regulatory role for this cell subset on non-immune cells in the context of T. cruzi infection Looking into this phenomenon, Lieke et al [67] corroborated that it is mediated by IFN-γ secretion from NK cells, which induces an increase in iNOS expression in the fibroblasts. Peripheral and cord blood experimental infection assays highlighted NK cells as the most potent IFN-γ producing subset, besides secreting IL-15 [69] in response to the pathogen, suggesting their relevance in the primary response to infection
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