Abstract
Acute infection with Trypanosoma cruzi usually subsides spontaneously but the mortality rate encountered in individuals with the chronic infection is high. Much evidence has accumulated in the last five years that autoimmunity plays an important role in the pathogenesis of the myocarditis that is common in the chronic phase. A negative relationship has been observed between the demonstrable parasitaemia and the presence of severe cardiac lesions. This myocarditis is characterized by lymphocytic infiltrates and destruction of normal heart cells, in the absence of the parasite in situ. Furthermore, the demonstration in vitro of heart cell lysis by T. cruzi-sensitized T lymphocytes is strong evidence of autoimmunity in Chagas' disease.
Acquired immunity plays a major role in the course that T. cruzi infections may run in the mammalian host. As a result of the immune mechanisms induced by the parasite, the infection is controlled at subpatent levels, and the immune host does not develop acute T. cruzi infection again. At present there are several means of achieving immunoprotection against experimental T. cruzi infections, but it is not known whether vaccinated animals might develop chronic Chagas' disease and die many months or years later. Studies on immunoprotection against Chagas' disease should therefore not be limited only to the acute phase of the infection. Furthermore, the involvement of autoimmunity in the production of the lesions of Chagas' disease indicates that research in this area should be conducted with caution. The definition of an animal model for chronic Chagas' disease is essential to further development of immunological research devoted to immunoprophylaxis.
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Selected References
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