Abstract
Infection of mice with Trypanosoma cruzi produces pathological change which in many ways parallels the evolution of Chagas' disease in human patients. An essential element in this experimental pathology is the intense denervation observed during the resolution of acute-stage parasitaemia. Host cells, from a variety of tissues, have been shown to absorb parasite antigens and thus to become targets for the hosts' own anti-parasite immune response. The definition of common antigenic determinants, shared by T. cruzi and human neuronal cells, might explain why the electrical conduction systems and the autonomic nervous system are especially vulnerable to the postulated autoimmune process. We have the models, the tools and the hypotheses, and now we await the proof.