de Oliveira G A, Gattass C R
Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Brazil.
Immunol Lett. 1991 Jun;28(3):227-32. doi: 10.1016/0165-2478(91)90008-x.
Monoclonal antibodies directed against the Thy-1 molecule or the CD3 complex were used to analyze the activation of T cells from mice acutely infected with Trypanosoma cruzi. When stimulated with G7, a mitogenic anti-Thy-1 monoclonal antibody, spleen cells from infected mice showed a markedly reduced or absent response that could not be restored by varying the culture time or the antibody concentration. However, cells from acutely infected animals proliferated to 145-2C11, an anti-CD3 monoclonal antibody. Flow cytometric analysis showed that the impaired response to G7 could not be attributed to a lack of expression of Thy-1 or CD3. Indeed, G7 seemed to deliver a positive signal to the cells since the proliferative response was completely restored by the addition of PMA. Moreover, purified T cells from infected mice responded to G7 in the presence of accessory cells from uninfected animals. These results suggest that a defective co-stimulatory cell function could be involved in the immunosuppression. In addition, our data present evidence against a generalized T cell anergy in the acute phase of the disease, since CD3-mediated activation was normal.
针对Thy-1分子或CD3复合物的单克隆抗体被用于分析来自急性感染克氏锥虫小鼠的T细胞的激活情况。当用促有丝分裂的抗Thy-1单克隆抗体G7刺激时,感染小鼠的脾细胞显示出明显降低或无反应,且通过改变培养时间或抗体浓度无法恢复。然而,急性感染动物的细胞对抗CD3单克隆抗体145-2C11有增殖反应。流式细胞术分析表明,对G7反应受损不能归因于Thy-1或CD3表达的缺乏。事实上,G7似乎向细胞传递了一个阳性信号,因为添加佛波酯(PMA)后增殖反应完全恢复。此外,来自感染小鼠的纯化T细胞在存在未感染动物的辅助细胞时对G7有反应。这些结果表明,共刺激细胞功能缺陷可能参与了免疫抑制。此外,我们的数据提供了反对疾病急性期普遍存在T细胞无反应性的证据,因为CD3介导的激活是正常的。