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Chapter 21, 22, 23 & 24
Hypersensitivity – Type 1~4
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Four types of hypersensitivity reaction
IgE
Regulation of IgE response
Allergen
Mast cells and basophils
Genetics of allergic disease
Inflammatory response in asthmatic bronchi
Hyposensitization therapy
New treatments for allergic disease
The biological role of immediate hypersensitivity
Antibody dependent cytotoxicity
Frustrated phagocytosis
Chapter 21, 22, 23 & 24
Hypersensitivity – Type 1~4 (continued)
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ABO blood group antigens and transfusion reactions
Haemolytic disease of the newborn due to Rh incompatibility
Autoimmune haemolytic anaemias
Myasthenia gravis
Three categories of immune-complex disease
Mechanisms in type III hypersensitivity
Arthus reaction
Immune complex clearance and deposition
Three varieties of type IV hypersensitivity
Mechanisms in type IV hypersensitivity
Granulomatous hypersensitivity
Figure 10-2
Figure 10-12
Figure 10-14
Characteristics of IgE (reagin) antibody
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Heat labile (56oC, 30 min.)
Lowest serum concentration
Relatively abundant in mucosal secretions
Homocytotropic for mast cells and basophil
Figure 10-17
Immediate and late phase bronchial reactions
• Eosinophils play a central role for inflammatory cell
infiltration during the late-phase reaction
• Bronchial hyper-reactivity is associated with asthma
Factors involved in the development of allergy
• T cell deficiency is associated with atopy
• Environmental pollutants act to increase antigenspecific IgE
• The concept of allergic breakthrough (the presence
of concomitant factor, 'X', such as viral infections of
the upper respiratory tract, transient IgA deficiency
or decreased T suppresser cell activity, which
unrestrained IgE responses and clinical symptoms to
develop.
Treatment from the point of interrupting the IgE
mediated hypersensitivity
• Antigen removal
• Hyposensitization therapy, desensitized with antigen to
produce IgG and stimulate the Ts whilst the IgE level tend
to fall. The IgG will compete for IgE to interrupt the Ag-IgE
trigger on mast cell.
• Cromolyn is to inhibit the release of mediators of mast cell
probably because it can stabilize the mast cell membrane.
• Antihistamine is the competitor of histamine on tissue.
• Pharmacological drug to decrease the effect of allergy.
Why do complexes deposit, and why do the complexes show
affinity for particular tissues in different diseases?
• Increase of vascular permeability trigger the tissue deposition.
• High blood pressure and turbulence localize the deposition.
• Affinity of antigens for specific tissue can direct complexes to
particular sites. e.g. collagen of the basement membrane with
DNA-anti-DNA in SLE.
• Large complexes become deposited on the glomerular basement
membrane, while small complexes pass through.
• The class of immunoglobulin can influence the deposition of
immune complexes.
Figure 6-21