THE ROLE OF INTERLEUKIN-17 IN CHAGAS DISEASE: IMMUNOPATHOLOGICAL IMPLICATIONS IN CHAGAS CARDIOMYOPATHY
Keywords:
Th17 Cells, Inflammatory Cytokines, Myocardial Fibrosis, Chronic Inflammation, Immune ResponseAbstract
Chagas disease is a systemic infectious disease caused by the protozoan Trypanosoma cruzi, representing a significant public health problem in Brazil and other Latin American countries. Its main chronic clinical manifestation is Chagas cardiomyopathy, responsible for high morbidity and mortality rates and a significant reduction in the quality of life of affected individuals. Scientific evidence indicates that the progression of cardiac involvement is closely related to the host's immune response, especially to chronic inflammation mediated by cytokines. In this context, interleukin-17 (IL-17), a cytokine characteristic of the Th17 cell-mediated immune response, has been extensively investigated due to its role in modulating the inflammatory response and the immunopathological mechanisms of Trypanosoma cruzi infection. This study aimed to analyze the role of IL-17 in Chagas disease, with emphasis on its immunopathological implications in the development of Chagas cardiomyopathy. This is an integrative literature review, conducted in national and international databases, including original studies, reviews, and institutional documents relevant to the topic. It was found that IL-17 plays an ambiguous role in the evolution of Chagas cardiomyopathy, potentially contributing both to infection control and preservation of ventricular function, and to the perpetuation of chronic inflammation and the progression of myocardial fibrosis, depending on the immunological context, age group, and individual genetic factors. Therefore, IL-17 constitutes a central mediator in the clinical heterogeneity of Chagas cardiomyopathy, representing a potential prognostic marker and a promising target for immunomodulatory therapeutic strategies.
Downloads
Published
Issue
Section
License

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.