Immunotherapy for virus infection.
Immunotherapy for virus infection.
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病毒感染的免疫治疗。
DOI：
10.1007/978-3-642-71726-0_9
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发表时间：
1987
影响因子：
--
通讯作者：
Oldstone,MB
中科院分区：
文献类型：
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作者：
Oldstone,MB
对病毒引起的免疫反应疾病和相关免疫病理学的理解源于 Rowe (1954) 报道的研究。他表明，抑制免疫反应将淋巴细胞性脉络丛脑膜炎病毒（LCMV）通常致命的急性感染转变为易感小鼠的持续感染。许多研究者随后的工作使用了新生儿胸腺切除术、遗传性无胸腺小鼠、辐射、抗淋巴药物或抗胸腺细胞血清等（Buchmeeeret al. 1980 综述）扩展了病毒感染过程中免疫反应介导损伤的概念。此后，描述了淋巴细胞在介导病毒诱导的免疫损伤中的作用。首先，由 Lundstedt (1969) 和 Oldstone 等人独立进行的实验。 (1969) 表明，急性 LCMV 感染或初次接种后 6-9 天获得的淋巴细胞可在体外杀死 LCMV 感染的靶标。接下来，发现此类淋巴细胞源自胸腺并在其表面带有Thy 1.2标记（Coleet al.1973；MarkerandVolkert1973）。 (1972a, b) 表明，由于免疫抑制而在通常致死剂量的 LCMV 中存活的小鼠会发展为急性淋巴细胞性脉络膜脑膜炎 (LCM) 疾病，并在用同基因免疫 T 淋巴细胞重建时死亡。ZinkernagelandDoherty (1974 a) 定义了溶细胞 T 淋巴细胞与其感染目标之间需要两个信号，即病毒特异性和 H-2 限制，因此可以继续杀死 LCMV 感染的细胞。
Understanding of virus-induced immune response disease and the related immunopathology has its roots in the studies reported byRowe(1954). He showed that suppression of immune responses changed the ordinarily lethal, acute infection with lymphocytic choriomeningitis virus (LCMV) to a persistent infection in susceptible mice. The subsequent work of many investigators who used neonatal thymectomy, genetically athymic mice, irradiation, antilymphoid drugs, or antithymocyte sera, etc. (reviewed inBuchmeeeret al. 1980) extended the concept of immune response-mediated injury during viral infection. Thereafter, the role of lymphocytes in mediating virus-induced immunologic injury was delineated. First, experiments performed independently byLundstedt(1969) andOldstoneet al. (1969) showed that lymphocytes obtained 6–9 days after an acute LCMV infection or primary inoculation killed LCMV-infected targets in vitro. Next, such lymphocytes were found to be of thymic origin and to bear Thy 1.2 markers of their surfaces (Coleet al. 1973;MarkerandVolkert1973).Gildenet al. (1972a, b) showed that mice which survived an ordinarily lethal dose of LCMV owing to immunosuppression developed acute lymphocytic choriomeningitis (LCM) disease and died when reconstituted with syngeneic, immune T-lymphocytes.ZinkernagelandDoherty(1974 a) defined the need for two signals between the cytolytic T-lymphocyte and its infected target, namely, virus specificity and H-2 restriction, so that killing of LCMV-infected cells could proceed.