An antigen that does not normally circulate in the blood may become exposed to the immune system

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Thyroglobulin protein that is normally trapped within the thyroid follicles, for example, can stimulate the production of autoantibodies that cause the destruction of the thyroid; this occurs in Hashimoto's thyroiditis. Similarly, autoantibodies developed against lens protein in a damaged eye may cause the destruction of a healthy eye (in sympathetic ophthalmia).

2. A self-antigen that is otherwise tolerated may be altered by combining with a foreign hapten. The disease thrombocytopenia (low platelet count), for example, can be caused by the autoimmune destruction of thrombocytes (platelets). This occurs when drugs such as aspirin, sulfonamide, antihistamines, digoxin, and others combine with platelet proteins to produce new antigens. The symptoms of this disease usually disappear when the person stops taking these drugs.

3. Antibodies may be produced that are directed against other antibodies. Such interactions may be necessary for the prevention of autoimmunity, but imbalances may actually cause autoimmune diseases. Rheumatoid arthritis, for example, is an autoimmune disease associated with the abnormal production of one group of antibodies (of the IgM type) that attack other antibodies (of the IgG type). This contributes to an inflammation reaction of the joints characteristic of the disease.

Table 15.10 Some Examples of Autoimmune Diseases



Postvaccinal and postinfectious encephalomyelitis

Myelin, cross-reactive



Sympathetic ophthalmia


Hashimoto's disease


Graves' disease

Receptor proteins for TSH

Autoimmune hemolytic disease

I, Rh, and others on surface of RBCs

Thrombocytopenic purpura

Hapten-platelet or hapten-absorbed antigen complex

Myasthenia gravis

Acetylcholine receptors

Rheumatic fever

Streptococcal, cross-reactive with heart valves


Streptococcal, cross-reactive with kidney

Rheumatoid arthritis


Systemic lupus erythematosus

DNA, nucleoprotein, RNA, etc.

Diabetes mellitus (type 1)

Beta cells in pancreatic islets

Multiple sclerosis

Components of myelin sheaths

Source: Modified from James T. Barrett, Textbook of Immunology, 5th ed. Copyright © 1988 Mosby-Yearbook. Reprinted by permission.

Source: Modified from James T. Barrett, Textbook of Immunology, 5th ed. Copyright © 1988 Mosby-Yearbook. Reprinted by permission.

The Immune System 471

4. Antibodies produced against foreign antigens may cross-react with self-antigens. Autoimmune diseases of this sort can occur, for example, as a result of Streptococcus bacterial infections. Antibodies produced in response to antigens in this bacterium may cross-react with self-antigens in the heart and kidneys. The inflammation induced by such autoantibodies can produce heart damage (including the valve defects characteristic of rheumatic fever) and damage to the glomerular capillaries in the kidneys (glomerulonephritis).

5. Self-antigens, such as receptor proteins, may be presented to the helper T lymphocytes together with class-2 MHC molecules. Normally, only antigen-presenting cells (macrophages, dendritic cells, and antigen-activated B cells) produce class-2 MHC molecules, which are associated with foreign antigens and recognized by helper T cells. Perhaps as a result of viral infection, however, cells that do not normally produce class-2 MHC molecules may start to do so and, in this way, present a self-antigen to the helper T cells. In Graves'disease, for example, the thyroid cells produce class-2 MHC molecules, and the immune system produces autoantibodies against the TSH receptor proteins in the thyroid cells. These autoantibodies, called TSAb's for "thyroid-stimulating antibody," interact with the TSH receptors and overstimulate the thyroid gland. Similarly, in type I diabetes mellitus, the beta cells of the pancreatic islets abnormally produce class-2 MHC molecules, resulting in autoimmune destruction of the insulin-producing cells.

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