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type II interferon 727 type III immune complex-mediated hypersensitivity
(a)
(b)
(c)
Opsonized
cell
C3b
IgG
C3b
receptor
Complement
activation
C1q
IgG
Target cell
Fc receptor
Phagocyte
C1q + C1r + C1s
C1, 4, 2, 3, 5b,
6, 7, 8, 9
with neuromuscular transmission results in muscular
weakness, ultimately affecting the muscles of respiration
and producing death. By contrast, stimulatory antibodies
develop in hyperthyroidism (Graves’ disease); they react
with thyroid-stimulating hormone receptors on thyroid
epithelial cells to produce hyperthyroidism.
type II interferon
Synonym for interferon-γ (IFN-γ).
type III immune complex-mediated hypersensitivity
A type of hypersensitivity mediated by antigen–antibody–complement
complexes. Antigen–antibody complexes
can stimulate an acute inflammatory response that
Formation
of
MAC
NK/K cell Perforin release
Surface antigen
Fc receptor
Ca 2+
IgG antibodycoated
target cell
NK/K cellmediated
lysis
Phagocytosed
cell
Phagocytosis
Antibody/
complementmediated
lysis
Forms of type II hypersensitivity. (a) Opsonization of cells by antibody and complement components and ingestion by phagocytes. (b) Antibody–
complement-mediated lysis of a nucleated cell as a consequence of formation of a membrane attack complex (MAC). (c) Antibody-dependent, cell-mediated
cytotoxicity through the action of a natural killer (NK) or killer (K) cell with surface antibody specific for a target cell.
Complement and Fc receptor-mediated inflammation
Fc
receptor
Complement activation
Complement Neutrophil
by products enzymes,
(C5a, C3a) reactive oxygen
intermediates
Inflammation and
tissue injury
Inflammation induced by antibody binding to Fc receptors of leukocytes and by complement breakdown products.
leads to complement activation and polymorphonuclear
neutrophil (PMN) leukocyte infiltration. The immune
complexes are formed by exogenous antigens such as
those from microbes or by endogenous antigens such as
DNA, a target for antibodies produced in systemic lupus
erythematosus (SLE). Immune complex-mediated injury
may be systemic or localized. In the systemic variety,
antigen–antibody complexes are produced in the circulation,
deposited in the tissues, and initiate inflammation.
Acute serum sickness occurred in children treated
with diphtheria antitoxin early in the 20th century as
a consequence of antibodies produced against horse
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