Regulation of complement activation
Complement activation does not occur in the fluid phase, but is localized on the surface of the organism, cell or immune complex that triggered the reaction. This is essential, as many of the by-products of complement activation are potent mediators of inflammation, and would cause extensive tissue damage if not controlled. In addition to the activation sequences described, there are regulatory proteins (factors H and I) that suppress the activation.
Effector function of complement
The most important effects of complement activation are:
DESTRUCTION OF PATHOGENS AND TUMOUR CELLS by the lytic process described above and by opsonizing them for phagocytosis
RECRUITMENT OF CELLS AND PROTEINS to inflammatory sites, by the chemoattractant activity of the proteolytic products CSa and C3a, and the increase in vascular permeability also p.c-iuced by these factors (sometimes called anaphylatoxins)
REMOVAL OF IMMUNE COMPLEXES by: opsonization,solubilization (alternative pathway) and prevention of precipitation (classical pathway)
IMMUNOMODULATION, especially B-cell responses Acute phase proteins Acute phase reactants are proteins that are synthesized in response to trauma, infection, necrosis, tumours or other inflammatory events. Although of secondary importance, these substances playa part in non-specific defence mechanisms and also appear to be involved in immunopathological processes. The measurement of creactive protein in the serum is used to monitor disease activity.
Heat shock proteins (HSPs)
HSPs are a family of highly conserved proteins which act as imrnunodominant antigens in many infections. They act as molecular chaperones, housekeeping proteins within cells, preserving the cell’s protein structure. They are involved in immunity. They are similar in configuration to antigens found on certain microorganisms and may induce autoimmunity through molecular mimicry.
SPECIFIC (ADAPTIVE) IMMUNITY
Specific immunity is the hallmark of the immune system. This is produced by a mechanism involving multiple rearrangements of original (germline) DNA in T and B lymphocytes. The altered DNA codes for proteins with hypervariable regions and creates the specific antigenbinding T-cell receptor and antibody molecules. This genetic diversity allows the production, for example, of over 108 different antibodies, enough to cover the spectrum of antigens encountered by humans.