Shirai T, Hirose S, Sekigawa I, Okada T, Sato H
J Rheumatol Suppl. 1987 Jun;14 Suppl 13:11-20.
There is now ample evidence that multiple genes are involved in the pathogenesis of systemic lupus erythematosus (SLE) in New Zealand mice. However, it also became evident that SLE is a syndrome in which each autoimmune feature is separately controlled by a limited number of major genes although some common genes do play a role in different autoimmune features. The data obtained by genetic analyses of murine lupus are a most useful guide for studies on autoimmunity, as related to (1) the type or subset of immune cells expressing each autoimmune disease gene; (2) how each gene or the cell (in which the gene is activated) plays a role in the etiopathogenesis of the disease; and (3) how the gene actions can be manipulated. Data on aspects of the genetic and cellular basis of murine lupus, particularly as related to the anti-DNA antibody synthesis in the (NZB X NZW)F1 hybrid mice are presented based on studies done in our laboratories.
现在有充分的证据表明,多个基因参与了新西兰小鼠系统性红斑狼疮(SLE)的发病机制。然而,同样明显的是,SLE是一种综合征,其中每个自身免疫特征分别由有限数量的主要基因控制,尽管一些共同基因确实在不同的自身免疫特征中发挥作用。通过对鼠类狼疮进行遗传分析获得的数据,对于自身免疫性研究是非常有用的指导,这涉及到:(1)表达每个自身免疫疾病基因的免疫细胞类型或亚群;(2)每个基因或(基因被激活的)细胞如何在疾病的病因发病机制中发挥作用;以及(3)基因作用如何被操控。基于我们实验室所做的研究,呈现了关于鼠类狼疮的遗传和细胞基础方面的数据,特别是与(NZB×NZW)F1杂交小鼠中抗DNA抗体合成相关的数据。