Kenyon R H, Peters C J
U.S. Army Medical Research Institute of Infectious Disease, Fort Detrick, Frederick, MD 21701-5011.
Microb Pathog. 1986 Oct;1(5):453-64. doi: 10.1016/0882-4010(86)90007-0.
Spleen cells from guinea pigs infected with an attenuated strain of Junin virus (the causative agent of Argentine hemorrhagic fever) specifically lysed virus-infected syngeneic target cells in vitro. This activity was detected as early as 6 days after infection, reached a maximum on days 10-13, and persisted at lower levels, at least through day 30. Monoclonal antibody to guinea pig T cells had no effect on the activity. After B or T cell enrichment techniques, the cytolysis was found with the B cell fraction. Aggregated IgG blocked the cytolysis. These characteristics suggested lytic activity was mediated at least in part by an antibody-dependent cell-mediated cytotoxicity (ADCC) mechanism. Although some cytolysis could be detected by using exogenously added antiserum and normal spleen effector cells, such reconstruction showed less efficient killing than when spleen cells from Junin-infected guinea pigs were used. This apparent discrepancy was resolved when spleen cells from these infected animals exhibited enhanced activity in non-viral ADCC systems as well. The cytotoxic activity by spleen cells against Junin-infected targets was detected only with non-fatal Junin infections. Cytolysis could not be measured in spleen cell suspensions from guinea pigs lethally infected with Junin virus; i.e. adults infected with a virulent strain of Junin and baby guinea pigs or immunosuppressed adult animals infected with an attenuated strain. However, spleen cells from both the immunosuppressed, infected adults and the adult guinea pigs infected with a virulent strain of Junin were able to mediate cytotoxicity in a nonviral system (antibody-sensitized Vero cells). The development of spleen cell cytotoxicity by Junin-infected guinea pigs against Junin-infected target cells correlated with whether the infection was resolved or was lethal.
感染了胡宁病毒减毒株(阿根廷出血热的病原体)的豚鼠脾细胞在体外能特异性裂解病毒感染的同基因靶细胞。这种活性最早在感染后6天就能检测到,在第10 - 13天达到最大值,并在较低水平持续至少到第30天。豚鼠T细胞单克隆抗体对该活性无影响。经过B细胞或T细胞富集技术处理后,发现细胞溶解作用存在于B细胞部分。聚集的IgG可阻断细胞溶解作用。这些特征表明,溶解活性至少部分是由抗体依赖性细胞介导的细胞毒性(ADCC)机制介导的。尽管使用外源性添加的抗血清和正常脾效应细胞也能检测到一些细胞溶解作用,但这种重建显示出的杀伤效率低于使用感染胡宁病毒的豚鼠脾细胞时的情况。当这些感染动物的脾细胞在非病毒ADCC系统中也表现出增强的活性时,这个明显的差异就得到了解决。只有在非致死性胡宁感染中,脾细胞对感染胡宁病毒的靶细胞才有细胞毒性活性。在感染致死剂量胡宁病毒的豚鼠脾细胞悬液中无法检测到细胞溶解作用;即感染强毒株胡宁的成年豚鼠以及感染减毒株胡宁的幼龄豚鼠或免疫抑制的成年动物。然而,免疫抑制的感染成年动物和感染强毒株胡宁的成年豚鼠的脾细胞在非病毒系统(抗体致敏的Vero细胞)中都能够介导细胞毒性。感染胡宁病毒的豚鼠脾细胞对感染胡宁病毒的靶细胞的细胞毒性发展与感染是得到解决还是致死相关。