Teixeira A R
Bull World Health Organ. 1979;57(5):697-710.
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.
克氏锥虫急性感染通常会自行消退，但慢性感染个体的死亡率很高。在过去五年中积累了大量证据表明，自身免疫在慢性期常见的心肌炎发病机制中起重要作用。已观察到可检测到的寄生虫血症与严重心脏病变的存在之间呈负相关。这种心肌炎的特征是淋巴细胞浸润和正常心脏细胞的破坏，而原位没有寄生虫。此外，克氏锥虫致敏的T淋巴细胞在体外对心脏细胞的裂解作用有力地证明了恰加斯病中的自身免疫。获得性免疫在克氏锥虫感染在哺乳动物宿主中可能经历的过程中起主要作用。由于寄生虫诱导的免疫机制，感染被控制在亚显性水平，免疫宿主不会再次发生急性克氏锥虫感染。目前有几种方法可以实现针对实验性克氏锥虫感染的免疫保护，但尚不清楚接种疫苗的动物是否会发展为慢性恰加斯病并在数月或数年后死亡。因此，针对恰加斯病的免疫保护研究不应仅局限于感染的急性期。此外，自身免疫在恰加斯病病变产生中的作用表明，该领域的研究应谨慎进行。慢性恰加斯病动物模型的定义对于致力于免疫预防的免疫学研究的进一步发展至关重要。
