小鼠内毒素反应的遗传控制。
Genetic control of endotoxic responses in mice.
作者信息
Watson J, Largen M, McAdam K P
出版信息
J Exp Med. 1978 Jan 1;147(1):39-49. doi: 10.1084/jem.147.1.39.
Abstract
A number of altered immunologic responses to lipopolysaccharide (LPS) in C3H/HeJ mice result from the expression in B lymphocytes of a defective genetic locus, termed Lps. Lps has been mapped to chromosome 4 between two loci, Mup-1 and Ps. As it is difficult to type individual mice for LPS responsiveness in more than one type of assay, we have utilized Mup-1 as a genetic marker to correlate LPS responses in mice to the expression of the Lps locus. Three nonlymphoid responses to LPS have been examined in 12 recombinant inbred strains of mice and in a backcross linkage analysis, and are all regulated by the expression of the Lps locus. These responses are hypothermal changes in body temperature, and the elevation in serum levels of a colony stimulating factor and the precursor of the secondary amyloid protein AA. Therefore, the initiation of LPS responses in different cell types in mice involve the expression of a common locus. These linkage studies provide a means for analyzing the genetic control of many of the diverse reactions of the endotoxic response to LPS.
摘要
C3H/HeJ小鼠对脂多糖（LPS）的多种免疫反应改变是由B淋巴细胞中一个有缺陷的基因位点Lps的表达引起的。Lps已被定位到4号染色体上Mup-1和Ps这两个位点之间。由于在多种检测中对单个小鼠进行LPS反应性分型很困难，我们利用Mup-1作为遗传标记，将小鼠的LPS反应与Lps位点的表达相关联。在12个重组近交系小鼠和回交连锁分析中检测了对LPS的三种非淋巴细胞反应，它们均受Lps位点表达的调控。这些反应包括体温的低温变化、集落刺激因子血清水平的升高以及继发性淀粉样蛋白AA前体的升高。因此，小鼠不同细胞类型中LPS反应的启动涉及一个共同位点的表达。这些连锁研究为分析内毒素对LPS反应中许多不同反应的遗传控制提供了一种方法。
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