Gegin C, Lehmann-Grube F
Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie, Universität Hamburg, Federal Republic of Germany.
J Immunol. 1992 Nov 15;149(10):3331-8.
For controlling infection of the mouse with the lymphocytic choriomeningitis (LCM) virus, CD8+ CTL are essential. In the infected BALB/c mouse the arising LCM virus-specific CTL are exclusively restricted by the class I MHC-encoded molecule L; K- or D-restricted antiviral CTL cannot be detected. Thus, the infected L-deficient BALB/c mutant C-H-2dm2 should not be capable of eliminating the virus. The experimental evidence proves the contrary, which is explained by K- and D-restricted CTL that this mouse generates. Why such cells remain undetectable in BALB/c mice is currently unexplained, because there is no lack of precursors and the corresponding virus Ag is presented. Despite the absence of lytic activity in vitro, other than the one associated with L, transfusion of day 8-immune spleen cells from BALB/c into infected C-H-2dm2 (L-deficient) mice results in accelerated virus elimination from the organs of the latter, which was manifest as soon as 8 h after cell transfer. Furthermore, lytic activity did not attain measurable levels in the recipients' spleens. Obviously, this infection can be terminated by CD8+ T lymphocytes even when these cells' lytic activity is below detectability.
对于控制小鼠感染淋巴细胞性脉络丛脑膜炎(LCM)病毒而言,CD8 + 细胞毒性T淋巴细胞(CTL)至关重要。在感染的BALB/c小鼠中,产生的LCM病毒特异性CTL仅受I类主要组织相容性复合体(MHC)编码分子L的限制;无法检测到受K或D限制的抗病毒CTL。因此,感染的L缺陷型BALB/c突变体C-H-2dm2应该无法清除病毒。然而实验证据却与之相反,这是由该小鼠产生的受K和D限制的CTL所解释的。目前尚无法解释为何此类细胞在BALB/c小鼠中无法被检测到,因为并不缺乏前体细胞且相应的病毒抗原也已呈递。尽管在体外除了与L相关的裂解活性外没有其他裂解活性,但将来自BALB/c的第8天免疫脾细胞输注到感染的C-H-2dm2(L缺陷)小鼠中会导致后者器官中的病毒加速清除,这种清除在细胞转移后8小时就很明显。此外,受体脾脏中的裂解活性并未达到可测量的水平。显然,即使这些细胞的裂解活性低于可检测水平,这种感染也可以被CD8 + T淋巴细胞终止。