New insights into the role of renal resident cells in the pathogenesis of lupus nephritis.

Author: Seung Ki KWOK ¹ ; George C TSOKOS
Author Information

1. Division of Rheumatology, Department of Internal Medicine, College of Medicine, Seoul St. Mary’s Hospital, The Catholic University of Korea, Seoul, Korea.
Publication Type:Review
Keywords: Systemic lupus erythematosus; Autoimmune diseases; Lupus nephritis; Podocytes
MeSH: Autoantibodies; Autoimmune Diseases; Biological Products; Epithelial Cells; Humans; Inflammation; Lupus Erythematosus, Systemic; Lupus Nephritis*; Mesangial Cells; Mortality; Podocytes
From:The Korean Journal of Internal Medicine 2018;33(2):284-289
CountryRepublic of Korea
Language:English
Abstract: Systemic lupus erythematosus (SLE), an autoimmune disease of unknown etiology, is characterized by the production of autoantibodies and end-organ damage. Lupus nephritis affects up to 70% of patients with SLE and is the most critical predictor of morbidity and mortality. The immunopathogenesis of SLE is complex and most clinical trials of biologics targeting immune cells or their mediators have failed to show efficacy in SLE patients. It has therefore become increasingly clear that additional, local factors give rise to the inflammation and organ damage. In this review, we describe recent advances in the role of renal resident cells, including podocytes, mesangial cells, and epithelial cells, in the pathogenesis of lupus nephritis.