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template theory (historical) 688 terminal complement components
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2.
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B
Antigen
B
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C
A
3. 6.
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C
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Antibody
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A
template theory (historical)
An instructive theory of antibody formation that requires
that antigen be present during antibody synthesis.
According to the refolding template theory, uncommitted
and specific globulins may become refolded on the antigen,
serving as a template for it. The cell thereupon releases
complementary antibodies that rigidly retain their shapes
through disulfide bonding. This theory was abandoned
when it became clear that the specificity of antibodies
in all cases is due to the particular arrangement of their
primary amino acid sequences. The template theory could
not explain immunological tolerance or the anamnestic
(memory) immune response.
tenascin
A matrix protein produced by embryonic mesenchymal
cells. It facilitates epithelial tissue differentiation and consists
of six identical 210-kDa proteins.
Terasaki, Paul (1929–)
American immunologist who began his career in transplantation
immunology as a postdoctoral research fellow under Peter
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Template theory.
Tenascin.
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B
C
Paul Terasaki, a pioneer in human histocompatibility.
Medawar in London in 1957. On returning to UCLA in 1959,
he perfected the microcytotoxicity test, which was important
in identification of the HLA system. He established the usefulness
of HLA in cross matching and detection of presensitization
in organ grafting. The principal theme of his research
has concerned evaluation of the role of HLA matching in
transplantation. His more recent work has been in establishing
the role of HLA antibodies in chronic rejection. Terasaki has
played a significant international role in tissue typing as director
of Tissue Typing at UCLA and directro of the Regional
Organ Procurement Agency in southern California. He is one
of the world’s leading researchers in HLA and transplantation.
The company he founded, One Lambda, Inc., has made key
contributions to HLA technology.
terminal complement complex
A sequence remains the same whether activation is initiated
via the classical, alternative, or lectin pathway. Following
cleavage of C5 by the classical or alternative C5 convertase,
the terminal complement components C6, C7, C8, and C9
are sequentially but nonenzymatically activated, resulting
in the formation of a terminal complement complex (TCC).
TCC can be generated on a biologic target membrane as
potentially membranolytic membrane attack complex
(MAC) or in extracellular fluids as nonlytic SC5b–9 in the
presence of S protein (also called vitronectin). Both forms
consist of C5b and the complement proteins C6, C7, C8,
and C9. Although some lytic activity is expressed by the
C5b–8 complex, efficient lysis is dependent on an interaction
with C9, facilitated by the α moiety of C8.
terminal complement complex (TCC) deficiency
The hereditary deficiency of a terminal complement component
leads to inability to form a functional terminal complement
complex with absence of hemolysis and bactericidal
activity. Patients with meningococcal infections frequently
exhibit terminal complement deficiencies, suggesting that
the cytolytic activity of the complement system is critical in
resistance to Neisseria meningitidis.
terminal complement components
The C5 through C9 constituents of the complement system that
assemble to produce the membrane attack complex (MAC).