The term immune complexes refers to antigen-antibody combinations that are free rather than attached to bacterial or other cells. The formation of such complexes activates complement proteins and promotes inflammation. This inflammation is normally self-limiting because the immune complexes are removed by phagocytic cells. When large numbers of immune complexes are continuously formed, however, the inflammation may be prolonged. Also, the dispersion of immune complexes to other sites can lead to widespread inflammation and organ damage. The damage produced by this inflammatory response is called immune complex disease.
Immune complex diseases can result from infections by bacteria, parasites, and viruses. In hepatitis B, for example, an immune complex that consists of viral antigens and antibodies can cause widespread inflammation of arteries (periarteritis). Arterial damage is not caused by the hepatitis virus itself but by the inflammatory process.
Immune complex disease can also result from the formation of complexes between self-antigens and autoantibodies. This produces systemic autoimmune disease, where the inflammation and tissue damage is not limited to a particular location. Two examples of this are the autoimmune diseases rheumatoid arthritis and systemic lupus erythematosus (SLE).
In rheumatoid arthritis, immune complexes in the synovial joints induce the activation of complement proteins and the se cretion of inflammatory cytokines. This leads to inflammation of the synovial joint and often leads to the progressive destruction of cartilage and bone. Such destruction is mediated by matrix metalloproteinase enzymes (chapter 6), released into the extracellular matrix in response to inflammatory cytokines secreted by helper T lymphocytes. Interestingly, antibodies of the IgM type are produced against the Fc portion of the person's own IgG antibodies! Such IgM autoantibodies are known as rheumatoid factor, and are diagnostic of rheumatoid arthritis.
People with SLE produce IgG autoantibodies against their own nuclear constituents, such as chromatin (DNA and protein), small nuclear ribonucleoprotein (snRNP)—described in chapter 3—and others. This can result in the formation of immune complexes throughout the body. In the glomerular capillaries (the filtering units of the kidneys, described in chapter 17), the inflammation provoked by the immune complexes can produce glomerulonephritis.
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