Chagas Disease: Navigating the Complexity of Host Immune Responses to Trypanosoma cruzi

Abstract

Trypanosoma cruzi is the source of the persistent systemic infection known as Chagas disease. There are various stages in its life cycle for both host mammals and vector insects. Along with regional variations in morbidity and mortality, distinct clinical presentations of Chagas disease are caused by distinct strains of Trypanosoma cruzi. The cytokine interferon-gamma is initially produced by natural killer cells during the early stages of T.cruzi infection. Cytokines secreted by phagocytes stimulate other defense-related cells and promote inflammation. In response to T. cruzi, B lymphocytes initiate an efficient humoral immune response, whereas dendritic cells, monocytes, and macrophages regulate the adaptive immunological response. This review includes several studies that address the primary immune mechanisms involved in T.cruzi infection, pathogen approaches against host cells, inflammasome, and virulence factor processes, and novel approaches to disease prevention, control, and treatment.