When antigen-antibody reactions take place in the blood, the consequences are directly related to the size of the immune complexes formed and the relative proportions of antigen and antibody therein (Figure 6.6). In antibody excess, the antigen becomes coated with antibody and is removed rapidly by cells of the mononuclear phagocyte system (using Fc and complement receptors). At antibody-antigen equivalence, large lattices are formed, their size enabling their rapid clearance. By contrast, when antigen is present in large excess (such as at the start of an infection, few antibody molecules coat each antigen thus reducing the likelihood of clearance. However, there is usually only a very brief period before specific antibody levels in the blood rise, resulting in the formation of immune complexes that contain equivalent or greater levels of antibody. However, in some instances, small immune complexes persist and these continue to circulate in the blood and may become localised in small blood vessels, e.g. in the glomeruli of the kidneys, the choroid plexuses, the joints and the ciliary body of the eye. It is thought that factors such as local high blood pressure and turbulent flow (glomeruli) or the filtering function of vessels involved (choroid plexus, ciliary body) may influence the deposition of these small immune complexes. In the glomeruli, they pass through the endothelium and may localise beneath the basement membrane, although the smallest appear to pass through the basement membrane and enter the urine. This may be a normal mechanism for disposing of such complexes.
Immune complexes that localise in the kidney glomeruli can activate complement and induce an inflammatory response. This results in poly-morphonuclear leukocyte infiltration, glomerular basement membrane swelling, and albumin and red blood cells in the urine. This acute glomerulonephritis may be seen mainly in children as a post-infection complication with Streptococcus spp. When the immune system has eliminated the infection, immune complexes are no longer formed and any pathological changes are usually reversed, leading to complete recovery. However, repeated infection or the persistent deposition of complexes leads to irreversible damage. This happens in certain persistent infections in which microbial
Figure 6.6 The influence of the structure of immune complexes on their clearance
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