- Author:
Young KIM
1
;
Seung Cheol SHIM
Author Information
- Publication Type:Review
- Keywords: Lupus nephritis; Apoptosis; Autoimmune diseases; Immunology; Lymphocytes
- MeSH: Adaptive Immunity; Allergy and Immunology; Antigen-Antibody Complex; Apoptosis; Autoantibodies; Autoimmune Diseases; Cell Death; Epigenomics; Genomics; Humans; Immunity, Innate; Inflammation; Lupus Nephritis*; Lymphocytes; Metabolomics; Microbiota; Models, Animal; Prognosis; Wolves*
- From:Journal of Rheumatic Diseases 2018;25(2):81-99
- CountryRepublic of Korea
- Language:English
- Abstract: Systemic lupus erythematous (SLE) is a systemic autoimmune disease with multi-organ inflammation caused by the production of pathogenic autoantibodies and immune complexes reflecting a global loss of tolerance. Lupus nephritis (LN) is present in approximately 60% of SLE patients and is considered a major predictor of a poor prognosis. To date, many studies utilizing genomics, transcriptomics, epigenetics, metabolomics, and microbiome have been conducted on a range of animal models and lupus patients to understand the pathogenesis of SLE and LN. Collectively, these studies support the concept that LN is caused by increased cell death, which has not been properly dealt with; abnormal innate immunity; hyperactive adaptive immunity; and genetic variants triggered by a range of environmental factors. This review summarizes the results from studies that contributed strongly to elucidating the pathogenesis of SLE and LN, highlighting the immunological and non-immunological mechanisms.