Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán.
Plan de Estudios Combinados en Medicina (PECEM), Facultad de Medicina, UNAM, Mexico City, Mexico.
Curr Opin Rheumatol. 2019 Mar;31(2):185-192. doi: 10.1097/BOR.0000000000000572.
The aim of this review is to discuss recent developments in our understanding of how systemic lupus erythematosus (SLE)-associated genes contribute to autoimmunity.
Gene-function studies have revealed mechanisms through which SLE-associated alleles of IFIH1, TNFAIP3, IRF5, and PRDM1 likely contribute to the development of autoimmunity. Novel research has identified Mac-1 (encoded by ITGAM), CaMK4, and iRhom2 as plausible therapeutic targets in lupus nephritis.
The work discussed in this review has broad implications for our understanding of the pathogenesis of SLE and for the development of novel therapeutic strategies.
本综述旨在讨论我们对系统性红斑狼疮(SLE)相关基因如何导致自身免疫的理解的最新进展。
基因功能研究揭示了 IFIH1、TNFAIP3、IRF5 和 PRDM1 的 SLE 相关等位基因可能导致自身免疫的机制。新的研究发现 Mac-1(由 ITGAM 编码)、CaMK4 和 iRhom2 是狼疮肾炎中合理的治疗靶点。
本综述中讨论的工作对我们理解 SLE 的发病机制和开发新的治疗策略具有广泛的意义。