Song Kangkang, Liu Lu, Zhang Xuejun, Chen Xiangmei
Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases, 28 Fuxing Road, Beijing, China.
Institute of Dermatology and Department of Dermatology at No.1 Hospital, Anhui Medical University, Key Laboratory of Dermatology, Ministry of Education (Anhui Medical University), Hefei, Anhui, China.
Clin Immunol. 2020 Jun;215:108389. doi: 10.1016/j.clim.2020.108389. Epub 2020 Mar 31.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by multiple system involvement and positive serum autoantibodies. Lupus nephritis (LN) is the most common and serious complication of SLE, and it is the main cause of death in patients with SLE. Abnormalities in the immune system lead to LN and involve a variety of cells (T cells, B cells, macrophages, NK cells, etc.), cytokines (interleukin, tumor necrosis factor α, etc.) and their related pathways. Previous studies have shown that the interactions of genetic, epigenetic and environmental factors contribute to the pathogenesis and development of LN. In recent years, one genome-wide association study (GWAS) and a number of gene association studies have explored the susceptibility genes of LN, including immunization-, inflammation-, adhesion- and other pathway-related genes. These genes participate in or suggest the pathogenesis and progression of LN. In this review, we summarize the genetic susceptibility of LN and discuss the possible mechanism underlying the susceptibility genes of LN.
系统性红斑狼疮（SLE）是一种慢性自身免疫性疾病，其特征为多系统受累以及血清自身抗体呈阳性。狼疮性肾炎（LN）是SLE最常见且最严重的并发症，也是SLE患者的主要死因。免疫系统异常导致LN，涉及多种细胞（T细胞、B细胞、巨噬细胞、NK细胞等）、细胞因子（白细胞介素、肿瘤坏死因子α等）及其相关途径。既往研究表明，遗传、表观遗传和环境因素的相互作用促成了LN的发病机制和发展。近年来，一项全基因组关联研究（GWAS）以及多项基因关联研究探索了LN的易感基因，包括免疫、炎症、黏附等途径相关基因。这些基因参与或提示了LN的发病机制和进展。在本综述中，我们总结了LN的遗传易感性，并讨论了LN易感基因潜在的可能机制。
