Rizzo L V, Cunha-Neto E, Teixeira A R
Laboratory of Immunopathology, MDC/Faculdade de Ciências da Saúde, Universidade de Brasília, Brazil.
Infect Immun. 1989 Sep;57(9):2640-4. doi: 10.1128/iai.57.9.2640-2644.1989.
In this study, we assessed the proliferative response of T cells from mice chronically infected with Trypanosoma cruzi to actin, myosin, or T. cruzi soluble antigen (SA). We report here that CD4+ T cells from mice chronically infected with T. cruzi proliferated in response to myosin but not to actin, whereas cells from naive mice did not proliferate against any of the antigens tested. Antisera raised against myosin- or SA-activated T cells specifically inhibited respectively, the myosin or SA in vitro proliferative response, whereas the response to unrelated antigen remained unimpaired. Sera from chronically infected mice failed to show any significant inhibitory activity. The above findings suggest that autoreactive and T. cruzi-reactive T cells belong to different, perhaps nonoverlapping, compartments of the immune cell repertoire of mice chronically infected with T. cruzi. The failure of infected mice to trigger the suppressive mechanisms described here might be the primary immune defect leading to breakdown of self-tolerance and unopposed, perhaps tissue-damaging, autoimmunity in experimental Chagas' disease.
在本研究中，我们评估了慢性感染克氏锥虫的小鼠T细胞对肌动蛋白、肌球蛋白或克氏锥虫可溶性抗原（SA）的增殖反应。我们在此报告，慢性感染克氏锥虫的小鼠的CD4 + T细胞对肌球蛋白有增殖反应，但对肌动蛋白无反应，而未感染小鼠的细胞对所测试的任何抗原均无增殖反应。针对肌球蛋白或SA激活的T细胞产生的抗血清分别特异性抑制了肌球蛋白或SA的体外增殖反应，而对无关抗原的反应则未受影响。慢性感染小鼠的血清未显示出任何显著的抑制活性。上述发现表明，自身反应性和克氏锥虫反应性T细胞属于慢性感染克氏锥虫的小鼠免疫细胞库中不同的、可能不重叠的亚群。感染小鼠未能触发此处描述的抑制机制可能是导致实验性恰加斯病中自身耐受性破坏和无对抗的、可能导致组织损伤的自身免疫的主要免疫缺陷。
