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type I cytokine receptors 725 type I cytokine receptors
IgE B cell
Antigen
IgE antibody
Ag
Primary and
secondary mediators
Mast cell
with IgE
Fc receptors
Type I hypersensitivity reaction in which antigen molecules cross link IgE
molecules on surfaces of mast cells, resulting in their degranulation and
release of primary and secondary mediators of anaphylaxis.
(a)
(b)
(c)
IgG
Target cell
Acetylcholine
receptor
C1q
IgG
Nerve
Muscle cell
Surface
antigen
NK/K cell
Fc Receptor
Surface antigen
Activation of
muscle
C1q + C1r + C1s
C1, 4, 2, 3, 5b,
6, 7, 8, 9
that induce allergy) attached to basophil or mast cell Fcε
receptors. Cross linking of the cell-bound IgE antibodies by
antigen is followed by mast cell or basophil degranulation
and the release of pharmacological mediators including vasoactive
amines such as histamine that causes increased vascular
permeability, vasodilation, bronchial spasm, and mucous
secretion. Secondary mediators of type I hypersensitivity
include leukotrienes, prostaglandin D 2, platelet-activating
factor, and various cytokines. Systemic anaphylaxis is a serious
clinical problem and can follow the injection of protein
antigens such as antitoxins or of drugs such as penicillin.
type I cytokine receptors
Cytokine receptors that possess conserved structural motifs
in their extracellular domains and bind cytokines that fold
into four α-helical strands. They include growth hormone,
interleukin-2 (IL2), IL3, IL4, IL5, IL6, IL7, IL9, IL11,
IL13, IL15, granulocyte–macrophage colony-stimulating
factor (GM-CSF), and G-CSF. Some of these receptors have
ligand-binding chains and one or more signal-transducing
chains. The same structural motifs are found in all these
chains. When bound to their cytokine ligands, type I
Formation
of
M.A.C.*
*Membrane attack complex
Acetylcholine
IgG
Perforin release
Ca 2+
NK/K cell
mediated lysis
IgG antibody
coated target
cell
Activation of
muscle inhibited
Antibody/
complement
mediated
lysis
Three forms of type II hypersensitivity.(a) Antibody and complement-mediated lysis of a nucleated cell as a consequence of formation of the membrane attack
complex (MAC). (b) 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. (c) Inhibition of transmission of nerve impulses by antibodies against acetylcholine receptors as occurs in myasthenia gravis.
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