ABSTRACT
Autoimmune disorders result when the immune system fails to discriminate between self and nonself, and thus produces autoantibodies that attack the body's own cells. Autoantibodies may be either specific (e.g., thyroid or blood autoantibodies) and associated with single-organ diseases or nonspecific (e.g., antinuclear antibodies) and associated with multi-system diseases (Oilier & Symmons, 1992). Autoantibodies do not necessarily destroy the target tissue; some achieve their effects by deranging the function of the organ or tissue (Crowley 1997). Many inflammatory granulomatous, degenerative, and atrophic disorders are now attributed to probable or possible autoimmune reactions. Among the more common of these disorders are multiple sclerosis (MS), rheumatoid arthritis (RA), Grave's disease, Hashimoto's thyroiditis, pernicious anemia, Type 1 diabetes mellitus, chronic active hepatitis, systemic lupus erythematosus (SLE), Sjogren's syndrome, glomerulonephritis, scleroderma, and myasthenia gravis (Carlson, Eisenstat, & Ziporyn, 1996; Crowley, 1997; Merck Research Laboratories, 1992; Oilier & Symmons, 1992). Chronic fatigue syndrome (CFS), irritable bowel syndrome (IBS), vasculitis, and other chronic disorders of unknown etiology are under investigation for evidence of autoimmunity (Oilier & Symmons, 1992). Together these disorders represent a significant proportion of the total incidence of chronic disease.
