Wong C Y, Woodruff J J, Woodruff J F
J Immunol. 1977 Apr;118(4):1165-9.
This report describes studies characterizing the virus-specific cytotoxic effector cells which are present in the spleens of mice 7 days after infection with Coxsackievirus B-3. An in vitro 51Cr assay employing eyngeneic virus-infected neonatal fibroblasts was used to measure cytotoxic activity. Treatment of immune cells with (anti-thy-1.2) and complement abolished dtheir cytotoxic activity, but no reduction occurred when B cells were removed by incubation with anti-Ig and complement or macrophages eliminated by adherence depletion. The findings therefore imply that the cytotoxic reaction was mediated by sensitized T cells and that B cells and macrophages did not play an important role. Reciprocal assays performed with BALB/c and CBA/J cells showed that Coxsackievirus-immune spleen cells lysed infected syngeneic targets but not allogeneic targets, providing further evidence that cytotoxicity was mediated by effector T cells. In addition and in vitro assay system employing neonatal myocardial cells was developed and used to demonstrate that Coxsackievirus-infected myofibers were susceptible to destruction by immune spleen cells. The evidence suggests that mice infected with Coxsackie B viruses are able to mount a cell-mediated immune response with production of cytotoxic T cells which have the capacity to damage tissues infected with these agents.
本报告描述了对感染柯萨奇病毒B - 3 7天后小鼠脾脏中存在的病毒特异性细胞毒性效应细胞的特性研究。采用同基因病毒感染的新生成纤维细胞的体外51Cr测定法来测量细胞毒性活性。用(抗thy - 1.2)和补体处理免疫细胞可消除其细胞毒性活性,但用抗Ig和补体孵育去除B细胞或通过贴壁去除巨噬细胞时,细胞毒性活性并未降低。因此,这些发现表明细胞毒性反应是由致敏T细胞介导的,而B细胞和巨噬细胞并未发挥重要作用。用BALB/c和CBA/J细胞进行的相互测定表明,柯萨奇病毒免疫的脾细胞可裂解感染的同基因靶细胞,但不能裂解异基因靶细胞,这进一步证明细胞毒性是由效应T细胞介导的。此外,还开发了一种采用新生心肌细胞的体外测定系统,用于证明柯萨奇病毒感染的肌纤维易受免疫脾细胞的破坏。证据表明,感染柯萨奇B病毒的小鼠能够产生细胞介导的免疫反应,产生具有损伤感染这些病原体组织能力的细胞毒性T细胞。