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antibody-dependent cell-mediated cyotoxicity (ADCC) 46 antibody feedback
Some may present clinically as severe combined immunodeficiency
with diminished cell-mediated immunity,
lymphopenia, and infection by microorganisms of low
pathogenicity. There are normal or even elevated numbers
of plasma cells, and there may be no demonstrable T cell
deficiency. Both findings are in contrast to the usual clinical
picture of severe combined immunodeficiency (SCID).
These individuals may develop autoimmune reactions and
show reduced numbers of lymphoid cells with surface
immunoglobulin in the circulating blood. One possible
explanation for normal immunoglobulin levels and an inadequate
humoral immune response to antigenic challenge
may be a defect in clonal diversity resulting in an antibody
response to only a limited number of antigens. Some investigators
have associated the defect with T cell clonal diversity.
This combined B and T cell system disorder resembles
SCID, but is less pronounced. Some patients with this defect
develop paraproteins with subsequent agammaglobulinemia
and clinical manifestations closely resembling SCID.
Lymphocyte
Antibody
ADCC.
Tumor cell
Tumor
cell lysis
antibody-dependent cell-mediated cyotoxicity (ADCC)
A reaction in which T lymphocytes, natural killer (NK)
cells (including large granular lymphocytes), neutrophils,
and macrophages may lyse tumor cells, infectious
agents, and allogeneic cells by combining through their
Fc receptors with the Fc regions of immunoglobulin G
(IgG) antibodies bound through their Fab regions to target
cell surface antigens. Following linkage of Fc receptors
with Fc regions, destruction of the target is accomplished
Antibody-binding site.
Antibody binding site
through released cytokines, representing an example of
participation between antibody molecules and immune
system cells to produce an effector function. NK cells
mediate most ADCC through the Fc receptor FcγRIII or
CD 16 on their surfaces.
antibody detection
Techniques employed to detect antibodies include immunoprecipitation,
agglutination, complement-dependent assays,
labeled anti-immunoglobulin reagents, blotting techniques,
and immunohistochemistry. Enzyme-based immunoassays,
blotting methods, and immunohistochemistry are routine
procedures to detect antibodies and characterize their
specificity.
antibody-directed enzyme pro-drug therapy (ADEPT)
A type of treatment in which an antibody is used to target
an enzyme to a tumor and unbound reagent is allowed to
clear. A nontoxic prodrug is then given and is activated by
the enzyme to form a cytotoxic drug at the tumor site. An
important part of ADEPT is bystander killing. Because the
drugs are activated extracellularly by the antibody–enzyme
complex, neighboring cells may also be killed by a mechanism
that does not require translocation across intracellular
membranes. By contrast, immunotoxins kill only the cells
to which they bind.
antibody-excess immune complexes (ABICs)
These complexes may result from alterations of the immunoglobulin
molecules such as those seen in rheumatoid
arthritis or may be produced locally as in type B hepatitis.
ABICs have a short intravascular life and, in contrast to
antigen-excess immune complexes, adhere to platelets and
cause platelet aggregation that is due not to crosslinking of
ABIC to platelets, but to changes in the adhesive properties
of the latter. ABICs also bind to neutrophils and induce
the release of lysosomal enzymes without prior phagocytic
activity.
antibody feedback
The negative feedback system whereby antigen-specific
antibodies downregulate further immune responses to