Infectious pathologies are a group of diseases that contribute with great impact on public health worldwide. Among the various diseases, some have a higher epidemiological importance, since their morbidity and mortality are very significant. In addition to the usual immune response, mounted against noxious agents, there is still the concept of infection-induced autoimmunity. Autoimmune diseases are defined as illnesses in which the evolution from benign to pathogenic autoimmunity takes place. However, proving a disease to be of autoimmune etiology is not a simple task. It is well known that both genetic influences and environmental factors trigger autoimmune disorders. However, some theories are still under great discussion. One of the most intriguing self-induced disorders is the hypothesis of autoimmunity during Chagas disease. Since the mid-1970s, the Chagas autoimmunity hypothesis has been considered an important contributor to the complex immune response developed by the host and triggered by Trypanosoma cruzi. New ideas and findings have strengthened this hypothesis, which has been reported in a series of publications from different groups around the world. The aim of this chapter is to discuss the mechanisms involving autoimmunity development during Chagas disease.
Part of the book: Physiology and Pathology of Immunology
For decades, non-human primates (NHPs) have been employed as experimental models to study many aspects of human diseases. They are the closest genetically to humans of any of the models applied in biomedical research; therefore, many authors have published scientific work regarding these animals and infectious diseases, including tuberculosis, AIDS, and tropical diseases. Among these, Chagas disease has caught the attention of many researchers all over the world. Recent studies have demonstrated great similarities with the human pathology, including cardiomyopathy and exacerbated pro-inflammatory response. Besides being genetically close to humans, NHP have a great probability to be naturally infected by Trypanosoma cruzi, which turns them into more interesting models to study Chagas disease mechanisms.
Part of the book: Primates