An update on genetic susceptibility in lupus nephritis.

Abstract

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.

• Authors: Kangkang Song, Lu Liu, Xuejun Zhang, Xiangmei Chen
• Journal: Clinical immunology (Orlando, Fla.) (Clin Immunol) Vol. 210 Pg. 108272 (01 2020) ISSN: 1521-7035 [Electronic] United States
• PMID: 31683055 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2019. Published by Elsevier Inc.

Topics

• Animals
• Autoimmunity
• Cell Adhesion (genetics)
• Gene-Environment Interaction
• Genetic Association Studies
• Genetic Predisposition to Disease
• Genome-Wide Association Study
• Humans
• Inflammation (genetics)
• Lupus Erythematosus, Systemic (genetics)