Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease of unknown etiology that primarily affects females during their child-bearing years. Genetic and environmental factors contribute to the development of this disorder, which is characterized by endogenous T- and B-cell activation, the appearance of multiple autoantibodies to self-constituents, immune complex formation, and inflammatory tissue injury in various organ systems. Consideration of stress proteins and the stress response as factors of possible etiopathogenetic significance in SLE came after the initial stress protein forays in adjuvant arthritis and rheumatoid arthritis (1), and this derives from the fortuitous detection of autoantibodies to heat shock proteins (hsps) 90 and 70 in SLE sera (2,3). Investigation during the past 5 years lies principally in three areas: (1) stress protein expression in and on cells of the immune system; (2) further definition of antibodies and autoantibodies to stress proteins; and (3) studies of a polymorphism of the hsp 70-2 gene, which is located in the class III region of the major histocompatibility complex (MHC). This chapter discusses the possible relevance of recent information in these areas to the pathogenesis of SLE.
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