Autoimmunity is an immunological reaction against constituents of an organism that normally is tolerated by the immune system of that organism. Autoimmune reactions can be either cell or antibody-mediated. Autoantibodies are therefore the antibodies that recognize normally tolerated cell and tissue constituents. The antigenic specificity of an autoantibody can be useful aid in clinical diagnosis. Autoantibodies are either cell specific, as found in organ-specific autoimmune disease such as autoimmune thyroiditis, or non-organ specific, as found in multisystems autoimmune disease, such as the systemic rheumatic diseases (Meyers, 1995 p.57).
The latter group includes autoantibodies that recognize macromolecular complexes of nucleic acids and/or proteins, such as small nuclear ribonucleoprotein particles (snRNPs), nucleosomal and subnucleosomal structures and tRNA synthetases, which are intrinsic components of all nucleated cell types present in an organism (Timby and Smith, 2006 p. 348). Autoimmunity results from a breakdown In the regulation in the immune system resulting in an inflammatory response directed at self-antigens and tissues. If ongoing. such a response leads to tissue destruction and Its resultant detrimental effects.
The pathological damage can be in one or several organs, or generalized In various tissues in the body (Pollard, 2006 p. 212). Organ-specific autoimmune diseases include the endocrinopathies, such as insulin-dependent diabetes mellitus (IDDM), and Hashimoto’s Thyroiditis. Generalized autoimmune disease is best exemplified by systemic lupus eythematosus (SLE). Between these extremes is a spectrum, containing a number of diseases with varying components of organ specificity . Discussion Autoimmune Diseases and Classifications
Autoimmune diseases are chronic disabling disorders in which immune deregulation leads the body to attack its own organs and tissues. More than 80 autoimmune diseases have been identified. The most common of these diseases include systemic lupus erythematosus (SLE). multiple sclerosis. type I diabetes, autoimmune thyroid diseases, myasthenia gravis, and rheumatoid arthritis (RA). Collectively, autoimmune diseases are thought to affect approximately 14—22 million people in the U. S. and represent a significant physical. emotional, social, and fiscal burden to the country’s health care system (Timby and Smith, 2006 p.349).
For reasons that are not clear, the prevalence of autoimmune diseases appears to be rising. Further, the development of effective therapies has lagged behind the growing prominence of these diseases (Pollard, 2006 p. 214). Autoimmune diseases form a large, heterogeneous group with a wide variety of clinical signs and symptoms. Despite this disparity, the immunopathology of all these diseases may be considered the result of particular hypersensitivity reactions, each disease being the result of one or more type of response (Meyers, 1995 p. 56).
Type II hypersensitivity responses usually involve autoantibody that recognizes either a normal (usually sequestered) or modified (by viruses or chemicals) cellular self-antigen. The resultant tissue damage gives rise to the signs and symptoms that are used in diagnosis of the disease, autoantibody may also interact with cellular receptors thus causing an abnormal expression of cellular activity (Timby and Smith, 2006 p. 349). Type Ill hypersensitivity reactions are seen in autoimmune diseases where the autoantibody binds to self-antigens free in tissue fluids or in the general circulation (Motze and Thomson, 2001 p.219).
The resulting complexes are free to circulate throughout the body. However, they may become quite large (depending on the relative concentrations of antibody and antigen) and therefore, insoluble (Pollard, 2006 p. 215). This results in their precipitation in the tissues and blood vessels. Particularly vulnerable are tissues with large filtering membranes such as the kidneys. joints and choroid plexus, where the presence of immune complexes results in the activation of the complement cascade and inflammatory sequelae (Meyers, 1995 p. 55).