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Autoimmunity is an immune response against self. It is a complex pathological condition in which the immune system recognizes and attacks the body's own tissue. Improper "Self-recognition" (or the ability of the immune system to distinguish between foreign proteins such as bacteria and viruses and the native tissues of the body) appears to underlie most of the autoimmune diseases.
The main job of the immune system is to distinguish between what is "self" and what is "not self". Once the distinction has been made, "self" should be pre-served and "non-self" is destroyed. The proper distinction between self and non-self is the reason that we are able to continue to live healthy lives. Recent scientific research suggests that the distinction between self and non-self is not absolute. This is evidenced by the occurrence of autoimmune disorders, the most common of which may effect up to 3% of the population. An autoimmune disorder is a pathology in which the immune system attacks normal, healthy tissue. Autoimmune disease, which may be crippling or fatal, can strike any tissue or organ. Its victims are often in the prime of life, and for unknown reasons they are more frequently women than men. Rheumatoid arthritis, for example, effects women 3 times more commonly than men.
Research on a form of autoimmune arthritis suggests that the basis of autoimmunity may be a resemblance between a specific foreign molecule and a molecule of the body. This finding is consistent with a model of the immune system in which the immune system receptors that perform the work of recognition can themselves be recognized by other receptors. Such "self-recognition," may form the basis of an equilibrium or homeostasis that keeps the body healthy. When this equilibrium is disrupted, as it is in autoimmunity, disease results.
In autoimmunity, self and the external world are no longer absolutely distinct. Current research is investigating types of vaccines that may ultimately ease the enormous suffering caused by autoimmune diseases. There are many different autoimmune diseases, also called IMID, or immune-mediated inflammatory diseases. IMIDs include multiple sclerosis, in which the tissue attacked is myelin (a substance that sheathes nerves in the central nervous system much like the insulation on electrical wiring in your home); myasthenia gravis, in which the target is a receptor molecule for the important neurotransmitter acetylcholine; rheumatoid arthritis, whose target is the collagen and bone within the peripheral joint; type I (juvenile) diabetes mellitus, in which the beta cells of the pancreas which produce insulin are destroyed, and systemic lupus erythematosus, in which DNA, blood vessels, skin and kidneys are attacked. In contrast to AIDS, (Acquired ImmunoDeficiency Syndrome) which is marked by an inactivation of T-cells which are key cells in the immune system.
In all these autoimmune diseases the immunological response is strong and well focused; it is, unfortunately, directed at some essential component of the body. These immunological attacks can be detected in the clinical laboratory by the measurement of tissue-specific and tissue non-specific antibodies.
Autoimmune diseases can be separated broadly into two categories. One group is characterized by the presence of auto-antibodies (antibodies against self) which are broadly reactive with nuclear or cytoplasmic antigens and do not demonstrate any tissue specificity. Included in this group are diseases such as rheumatoid arthritis, Lupus (SLE), mixed connective tissue disease, scleroderma, Sjogren’s syndrome, and dermatomyositis/polymyositis. A second group of autoimmune diseases is characterized by autoantibodies which demonstrate tissue specificity. These diseases include thyroiditis, chronic liver diseases (including primary biliary cirrhosis and chronic active Hepatitis), certain cases of pernicious anemia, and myasthenia gravis.
The autoantibodies which appear in these disease states demonstrate different degrees of specificity with respect to both tissue and species (i.e. man, chimpanzee, etc.). Tissue-specific autoantibodies include those which react against erythrocyte (red blood cell) stromalantigens, platelets, antihemophilic globulin, thyroid tissue and other tissues, and gamma-globulin (rheumatoid factor). Autoantibodies without tissue specificity include anti-nuclear antibodies (ANA), anti-nucleoprotien, anti-DNA (anti-dsDNA), and anti-cytoplasmic antibodies. Autoantibodies directed against the formed elements of the blood can induce disease by causing the destruction and removal of these cells from the circulation. It is far less certain whether other types of autoantibodies play pathogenic roles.
Most studies of autoantibodies in both humans and animals have concentrated on the reactivity of humoral (blood) constituents. The cell-mediated immune response is far more efficient in terms of tissue destruction. Since humoral antibodies have been shown, under appropriate circumstances, to prevent cell-mediated tissue damage, they may have a protective rather than a destructive function. There is presently no proof that autoantibodies detected in human disease represent a primary manifestation of the disease itself or a secondary event stimulated by an underlying, but unrelated, abnormality.
Four general mechanisms have been proposed in the pathogenesis of autoantibody production:
- Alterations in the structure or distribution of antigens;
- Formation of cross-reactive antibodies following exposure to extrinsic antigens;
- Release of sequestered antigens; and
- Abnormalities of immunologic responsiveness.
An assault on self through molecular mimicry or antigenic similarity between foreign antigens (virus, bacteria) and human tissue antigens may result in the development an autoimmune disease, and is presented in the following figure:
More information on the Immune System.
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