Autoimmune Disease
In order for the immune system to protect the body against attack by foreign organisms, it must be able to distinguish between the body’s own proteins (autoantigens) and proteins from foreign cells (foreign antigens). When the immune system turns against autoantigens, thus attacking its own tissues, the resulting condition is an autoimmune disease.
Common autoimmune diseases include:
-glomerulonephritis, which compromises the filtering ability of the kidney tubules
-Graves’ disease, which stimulates the thyroid to overproduce thyroid hormone
-rheumatoid arthritis, which destroys joint tissue
-myasthenia gravis, which interferes with nerve-muscle communication
-multiple sclerosis, which destroys the fatty myelin coating of nerves
-systemic lupus erythematosus, which attacks deoxyribonucleic acid (DNA), causing widespread damage in kidneys, heart, lungs, and skin
-juvenile onset (Type I) diabetes mellitus, which destroys the insulin- producing beta cells of the pancreas, resulting in inability to regulate blood sugar properly.
Theories of Autoimmunity
The cells involved in immune reactions are B lymphocytes (B cells), which develop in the bone marrow, and T lymphocytes (T cells), which develop in the thymus. Each lymphocyte carries a recognition site for a specific anti­gen and becomes activated when that antigen is encountered. During de­velopment, most of the lymphocytes that could recognize and destroy widely occurring autoantigens are deleted. Tissues bearing these autoantigens are generally safe from subsequent attack by the immune system unless either the autoantigen mutates or the immune system confuses the autoantigen with a foreign antigen. However, some tissue-specific autoantigens are un­available when lymphocytes are developing in the bone marrow or thymus, and so lymphocytes with receptors for those autoantigens remain viable, posing the threat of tissue destruction in autoimmune diseases.
It is not yet clear why these lingering, self-reactive lymphocytes do not trigger autoimmunity more often, or why autoimmunity occurs when it does. However, there is strong suspicion that infection may play an important role in genetically susceptible individuals. An infection causes the production of inflammatory chemicals. If these are present at the same time that a lym­phocyte is presented with its autoantigen by an antigen-presenting cell, the combination could activate self-reactive lymphocytes that were not deleted during development. Destruction of body tissues bearing those autoantigens would follow.
In another possible process, termed “molecular mimicry,” a foreign pro­tein bears such similarity to an autoantigen that B cell antibodies or cyto­toxic T cells specific for that foreign antigen cross-react with autoantigens, causing tissue destruction. Alternatively, the combination of a foreign anti­gen with a self-protein can form a new complex capable of activating ap­propriate T or B lymphocytes to destroy tissues containing the complex.
 
 References
Janeway, Charles A., Jr., Paul Travers, Mark Walport, and J. Donald Capra. Im­munobiology: The Immune System in Health and Disease, 4th ed. New York: Elsevier Science Ltd./Garland Publishing, 1999.
Marieb, Elaine Nicpon. Human Anatomy and Physiology, 5th ed. San Francisco: Ben­jamin Cummings, 2001.