autoimmune disease, any of a number of abnormal conditions caused when the body produces antibodies to its own substances. In rheumatoid arthritis, a group of antibody molecules called collectively RF, or rheumatoid factor, is complexed to the individual's own gamma globulin blood proteins; the circulating complex apparently causes tissue inflammation and muscle and bone deformities. In Hashimoto's thyroiditis, an inflammatory disease of the thyroid gland, antibodies are produced against the thyroid protein thyroglobulin. In some blood disorders, antibodies may be produced against the body's own red and white blood cells. Myasthenia gravis, a disease characterized by weakened muscles, is thought to have an autoimmune origin. In systemic lupus erythematosus it has been shown that individuals have antibodies to certain of their own body substances that for some reason are acting as antigens; these substances include the individual's own nucleic acids and cell organelles such as ribosomes and mitochondria. Lupus can cause dysfunction of many organs, including the heart, kidneys, and joints. Because lupus and certain diseases of probable autoimmune origin, e.g., scleroderma and dermatomyositis, affect collagen (connective tissue) throughout the body and blood vessels, they are referred to as collagen-vascular diseases. In rheumatic fever, the individual produces antibodies to antigens of streptococcal bacteria; it is believed that the streptococcal antigens are structurally similar to antigens of the heart and that antistreptococcal antibodies, combining with antigenic sites on the heart, damage the muscle and heart valves. Diseases of the immune system are currently treated by a variety of nonspecific immunosuppressive drugs and steroids.
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Publication information: Article title: autoimmune disease. Encyclopedia title: The Columbia Encyclopedia, 6th ed.. © 2012 The Columbia Electronic Encyclopedia © 2012, Columbia University Press. Licensed from Columbia University Press. Used with the permission of Columbia University Press. All Rights Reserved. Publisher: The Columbia University Press. Place of publication: Not available. Publication year: 2013.
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