Pathological lymphocyte activation by defective clearance of self‐ligands in systemic lupus erythematosus

• Published in: Rheumatology (Oxford, England) Vol. 42; no. 2; pp. 214 - 222
• Main Author: YASUTOMO, K
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.02.2003; Oxford Publishing Limited (England)
• Subjects: Autoantigens - immunology; Autoimmunity; Biological and medical sciences; Deoxyribonuclease I - genetics; Humans; Ligands; Lupus Erythematosus, Systemic - genetics; Lupus Erythematosus, Systemic - immunology; Lymphocyte Activation - immunology; Medical sciences; Mutation; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; T-Lymphocytes - immunology; Autoimmunity; Human; Immunopathology; Connective tissue disease; Skin disease; Cell function; Enzyme; Pathogenesis; Autoimmune disease; Esterases; Activation; Antigen; Autoantigen; Deoxyribonuclease I; Cell death; Systemic disease; T-Lymphocyte; Hydrolases; Lupus erythematosus; Disseminated; Mutation; Locus; Apoptosis
• ISSN: 1462-0324; 1462-0332
• DOI: 10.1093/rheumatology/keg081

Systemic lupus erythematosus (SLE) is one of the autoimmune diseases extensively studied by immunologists and physicians. The main focus regarding SLE pathophysiology has been placed on abnormal cell surface receptor function on lymphocytes. However, recent studies have revealed that defective clearance of apoptotic cells causes self‐antigen accumulation, which could trigger the activation of autoreactive lymphocytes. Thus, here we review current findings about the association of the defective clearance of autoantigens and SLE, focusing on mutations in the DNase I locus and their relationship to SLE.