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Complement (written as c') is one of the protective cascading systems in blood. A cascading system
comprises of a large number of components or subsystems which activate each other in a sequential
manner to produce a specified action. Four cascade systems of molecules are present in the plasma.
These are clotting, kinin, fibrinolytic and complement systems. Of these complement system is most
important in relation to infections. It is also the most complex comprising of about 25 proteins. It
can be activated in two different ways which are called as classical pathway and alternate pathway
of complement activation. The activated complement cascade culminates in three useful results-
phagocytosis, lysis and inflammation.
Immunologic activators IgM > IgGl, IgG3 > IgG2 IgA, IgE and some IgG
subclasses
Plant or bacterial
Staphylococcal protein A polysaccharides
C3a Anaphylatoxin
Immunoconglutinins
These are the antibodies that display a specificity towards antigenic determinants that are exposed
by fixed complement but which are unavailable in free complement. These are auto-antibodies since
these are produced by an animal against its own complement. These antibodies are produced during
activation of complement, Le. in infections and after immunization. In the course of complement
fixation, new antigenic determinants are exposed. These new sites appear to be in C3b, although
some experiments have suggested that they appear in C4b.
Conglutinin is a beta globulin and is activated by conglutinin activating factor (KAF) and combines
with haemolytically inactive C3b to cause haemagglutination of erythrocytes that have combined
with non-agglutinating quantities of antibody. This conglutinin-complement fixation test is a
sensitive indicator of a serologic reaction.
Complement Receptors
Four types are:
CR1: these are found on a variety of cells including erythrocytes, neutrophils, monocytes,
macrophages, B cells and T cells. Important roles assigned to the receptors are phagocytosis,
clearance of immune complexes, converting B cells into antibody secretors and may serve in soluble
form as a cofactor for Factor 1.
CR2: It binds to C3b, C3d and C3d-g. Apart from acting as receptor for E-B virus, no function of CR2
has been ascertained.
CR3: Like CR1, it has a wide cell distribution that includes macrophages, LGL, neutrophils and
erythrocytes.
Miscellaneous receptors for C protiens
Source of Complement
The main source for the complement proteins are the hepatocytes, epithelial cells of the gut, blood
monocytes and tissue macrophages. More than 90% of plasma C3, C6, C8 and C9 is synthesised in
liver.
Deficiency of Complement
Complement activity can be impaired by the absence of one or more of its protein components.
Impaired complement activity causes various diseases. Acquired diseases result from temporary
depletion of a complement protein; which subside when cells again become able to synthesise that
protein. Congenital complement deficiencies are due to permanent genetic defects that prevent
synthesis of one or more complement components. The most significant effect of complement
deficiencies is lack of resistance to infection. In patients with C3 deficiencies, chemotaxis,
opsonization and cell lysis are impaired.
Glomerulonephritis CI,C8
Meningococcal infections C6