Environment and systemic lupus erythematosus: an overview

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown etiology that manifests as a pleomorphic systemic disease mainly affecting females. The variety of autoantibodies found in the serum of patients indicate that SLE is an autoimmune disease, but the mechanisms leading to the aberrant responses are not clearly understood although it is thought that a number of genetic and environmental factors may be involved. Environmental (or non-genetic) exposures could include infectious agents, chemicals or other compounds capable of modulating immune responses such as occupational/environmental pollutants or drugs, and behavioural factors such as smoking and diet. Environmental exposures may lead to the production of autoreactive T cells and autoantibodies, the stimulation of pro- and antiinflammatory cytokines, and target end-organ damage, but are not so convincing as agents causing SLE. Exposure to viruses increases antibody titres, but these may be the result of polyclonal B cell activation. The amount and timing of exposure to different environmental factors may play a significant and complex role in the pathogenesis of SLE and other autoimmune diseases. A better understanding of the etiopathogenetic mechanism of SLE is required in order to clarify the multiple interactions between environmental exposures and genetic factors.