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macrophage 472 macrophage
INFγ
Macrophage
Fc receptor
to circulatory embarrassment. Patients often develop skin
hemorrhages, anemia, and neurological problems. This
condition is considered less severe than multiple myeloma.
macrophage
A large mononuclear phagocytic cell found in many tissues.
It is derived from monocytes in the blood and is active
in innate immunity and early phases of nonadaptive host
defense. It acts as a professional antigen-presenting cell and
TNFα
Reactive oxygen
metabolites and
lysosomal enzymes
Tumor cell
Epitope
IgG antibody
Tumor cell
lysis
Macrophage-mediated tumor cell lysis proceeds by several mechanisms. Activated macrophages express Fcγ receptors that anchor IgG molecules attached
to tumor cells but not normal cells, resulting in the release of lysosomal enzymes and reactive oxygen metabolites and leading to tumor cell lysis. Another
mechanism of macrophage-mediated lysis includes the release of tumor necrosis factor α (TNF-α) that may unite with its high affinity receptors on tumor
cell surfaces, resulting in lysis, or exert its effects on small blood vessels and capillaries of vascularized tumors, leading to hemorrhagic necrosis, producing
a localized Shwartzman-like reaction.
INFγ
Macrophage
MHC class II
receptor
CD4+
TCR
Increase in
MHC class II
receptors
Tumor cell
epitope
CD4 +
helper
T cell
IL-2
Cytotoxic
T lymphocyte
(CTL)
T cell
receptor
CD8+
MHC class I
receptor
Perforin and
granzymes
release
Macrophage-mediated tumor immunity.
Tumor cell
Tumor cell
lysis
MCP-1 released by smooth muscle and endothelial cells promotes the recruitment of monocytes and macrophages to the subendothelial cell layer.
Deposition of lipids within these monocytes and macrophages then leads to development of atherosclerotic lesions.
an effector cell in both humoral and cell-mediated immunity.
Interferon-γ (IFN-γ) activates macrophages to increase
their capacity to kill intracellular microorganisms. IFN-γ
activated and primed macrophages can engage in both antigen
presentation and costimulation. A combination of IFN-γ
and bacterial endotoxin may cause an activated macrophage
to become hyperactivated, i.e., become a triggered cytolytic
macrophage possessing increased activity against pathogens