Abstract
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterised by numerous autoantibodies, especially antinuclear antibodies and antibodies directed to double strand DNA. The heterogeneity of the clinical manifestations reflects the complexity of the disease pathogenesis. The pathogenesis is charcterised by an inflammatory process involving autoantibodies, and activated and autoreactive lymphocytes and deposits of immune complexes, complement and vasclar and parenchymal cellular infiltrates in numerous tissues. The aethiology is unclear but enviromental factors including sex hormones, ultraviolet light exposure and infections are of importance as well as a genetic predisposition with genetic polymorphisms in immunoglobulin Fc receptor genes, cytokine genes, complement genes, those genes that regulate apoptosis and HLA genes. This article reviews the current concepts of the pathogenesis of SLE.
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