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classical C3 convertase 177 classical pathway of complement activation
Immunoglobulin M (IgM) is the main antibody produced
first in a primary humoral response to thymus-dependent
antigens, with IgG produced later in the response. A
secondary antibody response to the same antigen results
in the production of only small amounts of IgM but much
larger quantities of IgG, IgA, or IgE antibodies. T helper
cell lymphokines have a significant role in controlling class
switching. Only heavy chain constant regions are involved in
switching, with the light chain type and heavy chain variable
region remaining the same. The specificity of the antigenbinding
region is not altered. Mechanisms of class switching
during B cell differentiation include the generation of
transcripts processed to separate mRNAs and the rearrangements
of immunoglobulin genes that lead to constant region
gene segment transposition. Membrane IgM appears first on
immature B cells, followed by membrane IgD as cell maturation
proceeds. A primary transcript bearing the heavy chain
variable region, μ chain constant region, and δ chain constant
region may be spliced to form mRNA that codes for each
heavy chain. Following stimulation of B cells by antigen and
T lymphocytes, class switching is probably attributable to
immunoglobulin gene rearrangements. During switching, B
cells may temporarily express more than one class of immunoglobulin.
Class switching in B cells mediated by interleukin-4
(IL4) is sequential, proceeding from Cμ to Cγ 1 to Cε.
IgG 1 expression replaces IgM expression as a consequence of
the first switch. IgE expression replaces IgG 1 expression as a
result of the second switch. TGF-β and IL5 have been linked
to the secretion of IgA.
C1
Activator
C1
C14
C142
C1423
C6, C7
C4 C4a
C2 C2b
C3 C3a
classical C3 convertase
A surface serine protease comprised of complement components
C4b2a, which splits C3 into C3a and C3b. It participates
in the classical pathway of complement activation.
classical C5 convertase
Refer to C5 convertase.
classical Hodgkin lymphoma
Classification includes 95% of Hodgkin lymphomas divided
into nodular sclerosis, mixed cellularity, lymphocyte-
C5
C567
C56789
Cytolysis
C8, C9
C5a
Classical pathway of complement activation.
IgG1
C1q
Red blood cell
IgG1
Red blood cell
C1r
IgG1
C1q
C1s
predominant, and lymphocyte-depleted subtypes.
Characterized by Reed–Sternberg cells that have a CD30 ± ,
CD15 + , CD20 - , CD45 - immunophenotype.
classical pathway
Refer to classical complement pathway.
classical pathway of complement activation
One of the three complement activation pathways. A
mechanism to activate C3 through participation by the
serum proteins C1, C4, and C2. Immunoglobulin M (IgM)
or a doublet of IgG may bind the C1 subcomponent C1q.
Following subsequent activation of C1r and C1s, the two
C1s substrates C4 and C2 are cleaved. This yields C4b
and C2a fragments that produce C4b2a, known as C3
convertase, and activate opsonization, chemotaxis of
leukocytes, increased permeability of vessels, and cell
lysis. Activators of the classical pathway include IgM, IgG,
staphylococcal protein A, C-reactive protein, and DNA.
C1 inhibitor blocks the classical pathway by separating C1r
and C1s from C1q. The C4-binding protein also blocks the
classical pathway by linking to C4b, separating it from C2a,
and permitting factor I to split the C4b heavy chain to yield
C4bi, which is unable to unite with C2a, thereby inhibiting
the classical pathway.
C4b
C2a
C3b
C1
C2b
C5a
C1r
IgG1
C3a
C6 C7 C8
C5b
LYSIS
C6
C1s
C4a
C8
C9
C9
Classical pathway of complement activation.
C2
C3
C5 C4
C