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immune costimulatory molecules 356 immune elimination
Ab
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Immune complex disease.
Immune complexes in renal glomerulus.
Immune complex disease (ICD). Electron dense deposits.
immune costimulatory molecules
B7-1 and B7-2 and the CD28 and CTLA-4 receptors
constitute one of the dominant costimulatory pathways that
regulate T and B cell responses. Although both CTLA-4
and CD28 can bind to the same ligands, CTLA-4 binds to
B7-1 and B7-2 with a 20- to 100-fold higher affinity than
CD28 and is involved in the downregulation of the immune
response. B7-1 is expressed on activated B cells, activated T
cells, and macrophages. B7-2 is constitutively expressed on
interdigitating dendritic cells, Langerhans’ cells, peripheral
blood dendritic cells, memory B cells, and germinal center
B cells. Both human and mouse B7-1 and B7-2 can bind to
either human or mouse CD28 and CTLA-4, suggesting that
conserved amino acids form the B7-1/ B7-2/CD28/CTLA-4
critical binding sites.
immune cytolysis
Complement-induced destruction or lysis of antibodycoated
target cells such as tumor cells. Immune cytolysis of
red blood cells is referred to as immune hemolysis. Immune
cytolysis also involves the destruction of target cells by
cytotoxic T lymphocytes or natural killer (NK) cells
(including K cells) through the release of perforins.
immune deviation
Antigen-mediated suppression of the immune response may
selectively affect delayed-type hypersensitivity (DTH), leaving
certain types of immunoglobulin responses relatively
intact and unaltered. This selective suppression of certain
phases of the immune response to an antigen without alteration
of others is termed immune deviation. It may involve
conversion of a T cell response involving T H1 cytokines that
induce cell-mediated immunity to a T H2 cytokine response
that induces synthesis of selected antibody isotypes. Split
tolerance or immune deviation offers an experimental
model for dissection of the immune response into its component
parts. It is necessary to use an antigen capable of
inducing formation of humoral antibody and development of
delayed-type hypersensitivity to induce immune deviation.
Because it is essential that both humoral and cellular phases
of the immune response be directed to the same antigenic
determinant group, defined antigens are required. Immune
deviation selectively suppresses delayed-type hypersensitivity
and IgG 2 antibody production. By contrast, immunologic
tolerance affects both IgG 1- and IgG 2 antibody production
and delayed-type hypersensitivity. For example, prior
administration of certain protein antigens to guinea pigs
may lead to antibody production. However, the subsequent
injection of antigen incorporated into Freund’s complete
adjuvant leads to deviation from the expected heightened,
delayed-type hypersensitivity and formation of IgG 2 antibodies
to result in little of either, i.e., negligible delayedtype
hypersensitivity and suppression of IgG 2 formation.
Recent advances in understanding of cytokines and T cell
subsets have rekindled interest in immune deviation with
the delineation of the T H1 and T H2 subsets of CD4 + effector
T lymphocytes, and a cellular framework for immune deviation
is available. Powerful cell-mediated (DTH) responses
occur when T H1 cells secreting interleukin-2 (IL2) and
interferon γ (IFN-γ) are preferentially activated under
the influence of macrophage-derived IL12. By contrast,
synthesis of most antibody classes is favored by stimulation
of IL4-secreting T H2 cells. Cross-inhibition of T H2 cells by
IFN-γ and T H1 cells by IL4 and IL10 reinforces deviation
down one rather than the other T cell pathway.
immune elimination
Accelerated removal of an antigen from the blood circulation
following its interaction with specific antibody and
elimination of antigen–antibody complexes through the
mononuclear phagocyte system. A few days following antigen
administration, antibodies appear in the circulation and
eliminate the antigen at a much more rapid rate than the rate
in nonimmune individuals. Splenic and liver macrophages
express Fc receptors that bind antigen–antibody complexes
and also complement receptors, which bind those immune