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© Dirk Biddle
Following exposure to an antigenic stimulus, antibodies are formed and complex (join or bind) with the antigen in the circulation. Normally these immune complexes are rapidly removed from the bloodstream. Either they are phagocytized (phagocytosis of immune complexes by macrophages can result in release of cytokines, such as IL-1 and TNFα, which initiate fever) or degraded in the liver and eliminated, unless the liver is sluggish or antigen penetration into the general circulation is at a level that overwhelms the liver's ability to degrade the remaining immune complexes. In these circumstances antibody/antigen complexes may continue to circulate. Eventually these circulating complexes become more antigenic and new antibodies may be formed to the original immune complex. This results in a bigger and harder to clear immune complexes. Thus, the immune response continues and possibly escalates. Systemic physiology becomes increasingly compensatory, and pathology can result. Immune complexes may also circulate until reaching certain sites, where local factors (eg; antigen excess in gravitational dependent areas) may cause them to deposit (or precipitate) and bind to the vessel wall, where they may cause damage. Such complexes may also localize to small vessels, resulting in local inflammation and vasculitis. The accumulation of immune complexes in the body is inhibitory to B-cells, T-cells and NK-cells.
Deposition of immune complexes in the glomerular basement membrane can lead to glomerulonephritis. By similar mechanisms arthritis may result. Rheumatoid arthritis has many characteristics of a local immune complex reaction, whereas Systemic lupus erythematosus has many clinical features of serum sickness (1). The presence of immune complexes (ICs), rarely seen in healthy blood, may in turn indicate the presence of disorders in which they play a role. Fluctuating immune complex levels may also correlate with a worsening or improvement of the disorder.
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