Many lines of evidence suggest that autoimmune diseases are the result of chronic immune activation in genetically susceptible individuals following specific environmental exposures. Although the rarity and heterogeneity of autoimmune diseases and the lack of understanding of pathogenetic mechanisms have inhibited progress in the field, genes encoding histocompatibility molecules, immunoglobulins, complement components, peptide transporter proteins, T-cell receptors, sex hormones, cytokines, and metabolic enzymes important in drug and toxin elimination, have been identified as risk factors for one or more autoimmune diseases. Novel molecular genetic techniques and epidemiologic approaches that subset diseases by demographics, clinical manifestations, serology, and environmental exposures, should further elucidate the environmental and genetic risk factors for these increasingly recognized multifactorial disorders.
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