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complement activation 187 complement-dependent cytotoxicity test
Classical pathway Alternative pathway
Antigen–antibody
complex
C1q
fix the first subcomponent, designated C1q. This is followed
in sequence by C1qrs, 4, 2, 3, 5, 6, 7, 8, and 9 to produce
lysis. The alternative pathway does not utilize C1, 4, and 2
components. Bacterial products such as endotoxin and other
agents may activate this pathway through C3. Numerous
biological activities are associated with complement
besides immune lysis, including the formation of anaphylatoxin,
chemotaxis, opsonization, phagocytosis, bacteriolysis,
hemolysis, and other amplification mechanisms.
Complement intermediates can opsonize cells; peptides
resulting from complement component cleavage (anaphylatoxins)
enhance inflammation and act as chemoattractants.
Activation of complement renders immune complexes
soluble and facilitates their clearance and promotes antigen
presentation, B cell activation, and memory.
C1
C1
C14
C142
C1423
C6, C7
C2
Activation unit
C4b, 2a Activation unit C3bBb(P) Activation unit
Activator
C4
C2
C3
C5
C567
C56789
Cytolysis
Recognition unit
C3a
C8, C9
Complement activation.
C4
C8
C4a, 2a3b
C4a
C2b
C3a
C5a
C5a
C5
Activator Initiation convertase
C5b + C6, C7, C8, C9
Complement activation.
Mg Factor B
++
C3bB
Properdin (P)
C3
C3b
C3b 2Bb(P)
Factor D
C3a
Membrane attack complex
formation (lytic unit)
complement activation
The initiation of a series of reactions involving the complement
proteins of plasma that may result in either the death
and elimination of a pathogenic microorganism or amplification
of the complement cascade effect.
complement components 1-9
Refer to C1-C9.
complement control protein (CCP) modules
Complement activity-regulating proteins that are similar
structurally. Refer also to regulators of complement activation
(RCA).
complement deficiency conditions
Inherited complement deficiencies are rare. In healthy
Japanese blood donors, only 1 in 100,000 persons had no C5,
C6, C7, and C8; no C9 was contained in 3 of 1000 individuals.
Most individuals with missing complement components
do not manifest clinical symptoms. Additional pathways
provide complement-dependent functions that are necessary
to preserve life. If C3, factor I or any segment of the alternative
pathway is missing, the condition may be life threatening
with markedly decreased opsonization in phagocytosis. C3 is
depleted when factor I is absent. C5, C6, C7, and C8 deficiencies
are linked with infections, mainly meningococcal or
gonococcal, that usually succumb to the bactericidal action
of complement. Deficiencies in classical complement pathway
activation are often associated with connective tissue or
immune complex diseases. Systemic lupus erythematosus
(SLE) may be associated with C1qrs, C2, or C4 deficiencies.
Patients with hereditary angioedema (HAE) have a deficiency
of C1 inactivator. A number of experimental animals
with specific complement deficiencies have been described,
such as C6 deficiency in rabbits and C5 deficiency in mice.
Acquired complement deficiencies may be caused by either
accelerated complement consumption in immune complex
diseases with a type III mechanism or by diminished formation
of complement proteins as in acute necrosis of the liver.
complement-dependent cytotoxicity test
An assay in which cells bearing surface epitopes are incubated
in vitro with antibodies of the homologous specificity.
After complement is added, cells expressing the antigen
C