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clathrin 178 clonal selection
clathrin
The principal protein enclosing numerous coated vesicles.
The molecular structure consists of three 180-kDa heavy
chains and three 30- to 35-kDa light chains arranged
into typical lattice structures comprised of pentagons or
hexagons. These structures encircle the vesicles. Associated
with receptor-mediated endocytosis.
Cleveland procedure
A form of peptide map in which protease-digested protein
products, with sodium dodecyl sulfate (SDS) present, are
subjected to SDS-PAGE. This produces a characteristic
peptide fragment pattern that is typical of the protein substrate
and enzyme used.
clinical trial
A four-phase process (I through IV) in which a sequence of
controlled tests of a drug, vaccine, or treatment of interest is
evaluated in human volunteers to establish its safety and efficacy
before being recommended for licensing for public use.
CLIP
The processed fragment of invariant chain. In the major histocompatibility
complex (MHC) class II transport pathway,
the peptide binding groove must be kept free of endogenous
peptides. The cell uses one protein, called invariant chain
(and its processed fragment CLIP) to block the binding site
until needed. HLA-DM facilitates release of CLIP peptides
and their exchange for antigenic peptides as they become
available. As long as CLIP remains in the binding groove,
antigenic peptides cannot bind.
clonal
The exclusive stimulation of only those lymphocyte clones
that express receptors for a specific antigen.
clonal anergy
The interaction of immune system cells with an antigen,
without a second antigen signal, that is usually needed for a
response to an immunogen. This leads to functional inactivation
of the immune system cells in contrast to the development
of antibody formation or cell-mediated immunity.
clonal balance
In explaining autoimmunity in terms of clonal balance, it
is convenient to describe it as an alteration in the helperto-suppressor
ratio with a slight predominance of helper
activity. Factors that influence the balance of helper to
suppressor cells include aging, steroid hormones, viruses,
and chemicals. The genetic constitution of the host and the
mechanism of antigen presentation are the two most significant
factors that govern clonal balance. Immune response
genes associated with major histocompatibility complex
(MHC) determine MHC class II antigen expression on
cells presenting antigen to helper CD4 + lymphocytes.
Thus, the MHC class II genotype may affect susceptibility
to autoimmune disease. Other genes may be active as
well. Antigen presentation exerts a major influence on the
generation of an autoimmune response. Whereas a soluble
antigen administered intravenously with an appropriate
immunologic adjuvant may induce an autoimmune response
leading to immunopathologic injury, the same antigen
injected intravenously without the adjuvant may induce no
detectable response. Animals rendered tolerant to foreign
antigens possess suppressor T lymphocytes associated with
the induced unresponsiveness. Thus, self tolerance may
be due, in part, to the induction of suppressor T cells. This
concept is called clonal balance rather than clonal deletion.
Self antigens are considered to normally induce mostly suppressor
rather than helper T cells, leading to a negative suppressor
balance in the animal body. Three factors with the
potential to suppress immune reactivity against self include
nonantigen-specific suppressor T cells, antigen-specific
suppressor T cells, and anti-idiotypic antibodies. Suppressor
T lymphocytes may leave the thymus slightly before the
corresponding helper T cells. Suppressor T cells specific for
self antigens are postulated to be continuously stimulated
and usually in greater numbers than the corresponding
helper T cells.
clonal deletion (negative selection)
The elimination of self-reactive T lymphocytes in the
thymus during the development of natural self tolerance.
T cells recognize self antigens only in the context of major
histocompatibility complex (MHC) molecules. Autoreactive
thymocytes are eliminated following contact with self
antigens expressed in the thymus before maturation is completed.
The majority of CD4 + T lymphocytes in the blood
circulation that survive clonal deletion in the thymus fail
to respond to any stimulus. This reveals that clonal anergy
participates in suppression of autoimmunity. Clonal deletion
represents a critical mechanism to rid the body of autoreactive
T lymphocytes. This is brought about by minor lymphocyte
stimulation (Mls) antigens that interact with the T cell
receptor’s V β region of the T lymphocyte receptor, thereby
mimicking the action of bacterial super antigen. Intrathymic
and peripheral tolerance in T lymphocytes can be accounted
for by clonal deletion and functional inactivation of T cells
reactive against self. In addition to central tolerance that
results from clonal deletion of T or B cells, whose antigen
receptors identify self antigens with high affinity as a mechanism
of negative selection, peripheral tolerance depends
on clonal deletion of mature naïve T cells that interact with
their homologous self peptide/MHC presented by immature
dendritic cells, which leads to the destruction of T cell
clones with the potential to induce autoimmunity.
clonal exhaustion
The division of an activated lymphocyte at such a rapid rate
in the presence of persistent antigen that its progeny can no
longer replicate, i.e., replicative senescence, prior to degeneration
of memory cells.
clonal expansion
Antigen-specific lymphocyte proliferation in response to
antigenic stimulation that precedes differentiation into
effector cells. It is a critical mechanism of adaptive immunity
that enables rare antigen-specific cells to proliferate
sufficiently to combat the pathogenic microorganisms that
provoked the response.
clonal ignorance
Lymphocytes that survive the principal mechanisms of self
tolerance and remain functionally competent but are unresponsive
to self antigens and do not cause autoimmune reactions.
clonal restriction
An immune response that is limited to the expression of a
few lymphoid cell clones.
clonal selection
Antigen-mediated activation and proliferation of members
of a clone of B lymphocytes bearing receptors for the antigen
or for complexes of major histocompatibility complex
(MHC) and peptides derived from the antigen in the case of
T lymphocytes. Refer to clonal selection theory.