从对小鼠模型的研究中深入了解系统性红斑狼疮的遗传基础和免疫发病机制。

Insights into the genetic basis and immunopathogenesis of systemic lupus erythematosus from the study of mouse models.

机构信息

Department of Immunology, University of Toronto, Toronto, ON, Canada.

出版信息

Semin Immunol. 2009 Dec;21(6):372-82. doi: 10.1016/j.smim.2009.10.005.

DOI:10.1016/j.smim.2009.10.005

PMID:19926489

Abstract

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease characterized by production of autoantibodies directed against nuclear antigens resulting in formation of immune complexes that deposit in multiple organs causing tissue damage. SLE is a complex genetic disease in which variations in multiple genes, each with a modest effect size, contribute to disease genesis. Given this genetic complexity, identification of the role of individual polymorphisms is challenging. In this context, studies of mouse models of lupus have been particularly informative. Here we review the findings arising from the study of gene deleted, transgenic and congenic lupus-prone mouse models.

摘要

系统性红斑狼疮（SLE）是一种多系统自身免疫性疾病，其特征是产生针对核抗原的自身抗体，导致形成免疫复合物，沉积在多个器官中，引起组织损伤。SLE 是一种复杂的遗传疾病，多个基因的变异，每个基因的影响都不大，导致疾病的发生。鉴于这种遗传复杂性，确定个体多态性的作用具有挑战性。在这方面，狼疮小鼠模型的研究特别有启发性。在这里，我们回顾了基因缺失、转基因和同基因狼疮易感小鼠模型研究的结果。