Bubbers J E, Blank K J, Freedman H A, Lilly F
Scand J Immunol. 1977;6(5):533-9. doi: 10.1111/j.1365-3083.1977.tb02117.x.
Evidence has been gathered which supports the notion that two distinct but interacting mechanisms, controlled by loci mapping within the H-2 complex, influence Friend murine leukemia virus (FV) disease. One mechanism, controlled by a gene mapping in or close to H-2D, influences the capacity of the H-2D gene product to form molecular complexes with FV molecules in the plasma membrane of infected cells. Formation of a complex appears to provide a target antigen for syngeneic cytotoxic T-lymphocytes, to cause co-capping of FV and H-2D antigens, to permit the selective inclusion of H-2Db molecules into progeny Friend virions, to influence the long-term maintenance of virus production in vitro and, in conjunction with the second mechanism, to stimulate the generation of cytotoxic T-lymphocytes. This second mechanism is controlled by a gene in the H-2K or H-2I region, and, in the presence of an H-2/FV molecular complex immunogen, influences the generation of H-2 restricted cytotxic T-lymphocytes and the rate of rejection of syngeneic FV-induced tumor cells.
已有证据支持这样一种观点，即由H - 2复合体内定位的基因座控制的两种不同但相互作用的机制影响Friend小鼠白血病病毒（FV）疾病。一种机制由定位在H - 2D内或其附近的基因控制，影响H - 2D基因产物在受感染细胞质膜中与FV分子形成分子复合物的能力。复合物的形成似乎为同基因细胞毒性T淋巴细胞提供了靶抗原，导致FV和H - 2D抗原的共帽化，允许H - 2Db分子选择性地纳入子代Friend病毒粒子，影响体外病毒产生的长期维持，并与第二种机制一起刺激细胞毒性T淋巴细胞的产生。第二种机制由H - 2K或H - 2I区域中的一个基因控制，并且在存在H - 2/FV分子复合免疫原的情况下，影响H - 2限制性细胞毒性T淋巴细胞的产生以及同基因FV诱导的肿瘤细胞的排斥率。
