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新西兰小鼠系统性红斑狼疮中抗DNA抗体合成的遗传和细胞基础。

Genetic and cellular basis of anti-DNA antibody synthesis in systemic lupus erythematosus of New Zealand mice.

作者信息

Shirai T, Hirose S, Sekigawa I, Okada T, Sato H

出版信息

J Rheumatol Suppl. 1987 Jun;14 Suppl 13:11-20.

PMID:3497267
Abstract

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.

摘要

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。

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