Gironès Núria, Carrasco-Marin Eugenio, Cuervo Henar, Guerrero Néstor Adrián, Sanoja Cristina, John Sparrow, Flores-Herráez Reyes, Fernández-Prieto Lorena, Chico-Calero Isabel, Salgado Hugo, Carrión Javier, Fresno Manuel
Centro de Biología Molecular, CSIC-UAM, Universidad Autónoma de Madrid, Cantoblanco, E-28049 Madrid, Spain.
Ann N Y Acad Sci. 2007 Jun;1107:434-44. doi: 10.1196/annals.1381.046.
Chagas disease, caused by Trypanosoma cruzi, affects several million people in Central and South America. About 30% of chronic patients develop cardiomyopathy probably caused by parasite persistence and/or autoimmunity. While several cross-reactive antibodies generated during mammal T. cruzi infection have been described, very few cross-reactive T cells have been identified. We performed adoptive transfer experiments of T cells isolated from chronically infected mice. The results showed the generation of cardiac pathology in the absence of parasites. We also transferred cross-reactive SAPA-specific T cells and observed unspecific alterations in heart repolarization, cardiac inflammatory infiltration, and tissue damage.
恰加斯病由克氏锥虫引起，影响中南美洲数百万人。约30%的慢性病患者会发展为心肌病，可能是由寄生虫持续存在和/或自身免疫所致。虽然在哺乳动物感染克氏锥虫期间产生的几种交叉反应性抗体已被描述，但已鉴定出的交叉反应性T细胞却很少。我们进行了从慢性感染小鼠中分离T细胞的过继转移实验。结果显示在没有寄生虫的情况下出现了心脏病理变化。我们还转移了交叉反应性的南美锥虫抗原特异性T细胞，并观察到心脏复极化、心脏炎性浸润和组织损伤的非特异性改变。
