Ertl H, Koszinowski U
Z Immunitatsforsch Immunobiol. 1976 Sep;152(2):128-40.
After injection of Sendai virus, a parainfluenza virus type I, mice generate cytotoxic lymphocytes which lyse specifically Sendai-virus-infected target cells in vitro. Their action is not inhibited by specific antibody in vitro. Killer cell activity appears 4 days after infection, reaches a maximum on the 7th day and disappears on the 14th to 16th day. Decrease of cytotoxic cell activity is correlated with an increase of haemagglutinating antibodies. The cytotoxic effector cell could be characterized as a thymus-derived cell, there is no specific activity in antibody-dependent cell-mediated cytolysis (ADCC). The degree of cytotoxic effector cell activity is only slightly influenced by the dose of injected infective virus. Using different syngeneic Sendai-virus-infected cells as targets for cell-mediated cytotoxicity, a tumor line was not lysed by cytotoxic lymphocytes in spite of viral surface antigens. Preliminary experiments were performed to demonstrate the H-2 gene restriction of the cytotoxic interaction. Using macrophages and tumor cells as targets only syngeneic infected target cells were lysed.
注射仙台病毒(一种I型副流感病毒)后,小鼠会产生细胞毒性淋巴细胞,这些细胞毒性淋巴细胞在体外能特异性地裂解被仙台病毒感染的靶细胞。它们的作用在体外不受特异性抗体的抑制。杀伤细胞活性在感染后4天出现,在第7天达到最大值,并在第14至16天消失。细胞毒性细胞活性的降低与血凝抗体的增加相关。细胞毒性效应细胞可被表征为胸腺来源的细胞,在抗体依赖性细胞介导的细胞溶解(ADCC)中没有特异性活性。细胞毒性效应细胞活性的程度仅受到注射的感染性病毒剂量的轻微影响。使用不同的同基因被仙台病毒感染的细胞作为细胞介导细胞毒性的靶标,尽管存在病毒表面抗原,但一种肿瘤细胞系未被细胞毒性淋巴细胞裂解。进行了初步实验以证明细胞毒性相互作用的H-2基因限制性。使用巨噬细胞和肿瘤细胞作为靶标,仅同基因感染的靶细胞被裂解。