Host genetic control of recovery from Friend leukemia virus-induced splenomegaly: mapping of a gene within the major histocompatability complex.
Host genetic control of recovery from Friend leukemia virus-induced splenomegaly: mapping of a gene within the major histocompatability complex.
复制标题
DOI：
10.1084/jem.140.6.1457
复制
发表时间：
1974-12-01
影响因子：
15.3
通讯作者：
Stimpfling, J
中科院分区：
文献类型：
--
作者：
Chesebro, B;Wehrly, K;Stimpfling, J
小鼠主要组织相容性基因复合体（H-2）对小鼠对Friend白血病病毒反应的影响在F1同源小鼠中进行了研究，仅在H-2复合体内的基因上存在差异。与H-2 B/d或H-2 B/a小鼠相比，H-2 B/B的F1小鼠脾肿大恢复的发生率较高。在H-2复合物内重组的小鼠中，发现负责Friend病毒恢复效应的基因（指定为RFV-1）在血清学可检测的移植抗原的D区域附近或内部作图。由于F1 H-2 B/B小鼠的恢复发生率远高于亲代H-2 B/B小鼠，因此其他非H-2宿主遗传因素似乎对H-2 B/B F1小鼠的恢复表达也很重要。这些基因的作用机制仍然未知。
The influence of the major mouse histocompatibility gene complex (H-2) on the response of mice to Friend leukemia virus was studied in F1 congenic mice differing only at genes within the H-2 complex. F1 mice which were H-2b/b had a high incidence of recovery from splenomegaly compared to H-2b/d or H-2b/a mice. In mice with recombinations within the H-2 complex a gene (designated RFV-1), responsible for the Friend virus recovery effect, was found to map near or within the D region of serologically detectable transplantation antigens. Because the incidence of recovery was much higher in F1 H-2b/b mice than in parental H-2b/b mice, other non-H-2 host genetic factors also appear to be important to expression of recovery in H-2b/b F1 mice. The mechanisms of action of these genes remain unknown.