Huber S A, Job L P, Woodruff J F
Am J Pathol. 1980 Mar;98(3):681-94.
Spleen cells from male adult BALB/c mice given intraperitoneal injections of purified coxsackievirus B-3 were examined for the ability to lyse syngeneic neonatal myofibers in culture. Cytotoxicity against infected and uninfected targets was measured with the use of an in vitro 51Cr release assay. Immune spleen cells obtained 4--7 days after infection were cytotoxic for viral-infected myofibers. Peak reactivity was observed 5 days after infection. At this time immune spleen cells showed significantly less reactivity against uninfected myofibers. Cytotoxicity against infected targets was mediated by T lymphocytes, since reactivity was abolished by treatment with anti-thy 1.2 and complement. Treatment with anti-Ig and complement caused no loss of activity. Reciprocal assays performed with BALB/c and CBA cells showed that maximal cytotoxicity occurred against infected syngeneic myofibers, providing further evidence that viral-specific effector cells were T lymphocytes. In addition, hyperimmune rabbit anti-coxsackievirus B-3 antiserum could not block immune spleen cell lysis of infected targets, suggesting that coxsackievirus-infected myofibers expressed surface membrane antigens not recognized by specific neutralizing antibody.
对腹腔注射纯化柯萨奇病毒B - 3的成年雄性BALB/c小鼠的脾细胞进行检测,观察其在培养物中裂解同基因新生肌纤维的能力。使用体外51Cr释放试验测定对感染和未感染靶细胞的细胞毒性。感染后4 - 7天获得的免疫脾细胞对病毒感染的肌纤维具有细胞毒性。感染后5天观察到反应峰值。此时,免疫脾细胞对未感染的肌纤维的反应明显降低。对感染靶细胞的细胞毒性由T淋巴细胞介导,因为用抗Thy 1.2和补体处理后反应性消失。用抗Ig和补体处理不会导致活性丧失。用BALB/c和CBA细胞进行的双向试验表明,对感染的同基因肌纤维产生最大细胞毒性,这进一步证明病毒特异性效应细胞是T淋巴细胞。此外,超免疫兔抗柯萨奇病毒B - 3抗血清不能阻断免疫脾细胞对感染靶细胞的裂解,这表明柯萨奇病毒感染的肌纤维表达了特异性中和抗体无法识别的表面膜抗原。