Wakeland E K, Wandstrat A E, Liu K, Morel L
Center for Immunology, University of Texas Southwestern Medical Center, Dallas 75235-9093, USA.
Curr Opin Immunol. 1999 Dec;11(6):701-7. doi: 10.1016/s0952-7915(99)00039-4.
Recent progress towards elucidating the genetic basis for susceptibility to systemic lupus erythematosus (SLE) has provided insights into the manner in which individual susceptibility genes contribute to disease pathogenesis. Studies in animal models of systemic autoimmunity suggest that genes in three separate pathways contribute to the initiation and progression of systemic autoimmunity. Linkage studies in humans suggest that at least some susceptibility genes mediating disease in lupus-prone mice may also contribute to susceptibility in humans.
在阐明系统性红斑狼疮(SLE)易感性的遗传基础方面的最新进展,为个体易感基因促成疾病发病机制的方式提供了见解。系统性自身免疫动物模型的研究表明,三个不同途径中的基因促成了系统性自身免疫的起始和进展。人类的连锁研究表明,至少一些在狼疮易感小鼠中介导疾病的易感基因也可能导致人类的易感性。