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Immunology Chapter 17. Richard L. Myers, Ph.D. Department of Biology Southwest Missouri State Temple Hall 227 Telephone: 417-836-5307 Email: Homepage: TopClass: Hypersensitivity reactions.

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immunology chapter 17
ImmunologyChapter 17
  • Richard L. Myers, Ph.D.
  • Department of Biology
  • Southwest Missouri State
  • Temple Hall 227
  • Telephone: 417-836-5307
  • Email:
  • Homepage:
  • TopClass:
hypersensitivity reactions
Hypersensitivity reactions
  • Generally, the immune response eliminates antigens without extensive damage to host
    • sometimes produce inflammatory response
    • can have deleterious effects like tissue damage
  • These reactions are called hypersensitive or allergic reactions
  • Occur during humoral or cell mediated response
gell and coombs classification
Gell and Coombs Classification
  • Several types of hypersensitivity reactions can be distinguished
  • Different mechanisms give rise to different reactions
    • Gell and Coombs proposed a classification
  • Divided them into 4 types
    • Types I, II, III and IV
Type I reactions are induced by antigens called allergens
  • Antibodies are produced by a normal route
    • Ab producing and memory cells
    • the normal cells secrete IgE
  • IgE binds to Fc receptors on the surface of mast cells and blood basophils
    • cells are sensitized
  • A later exposure to the same allergen cross-links membrane-bound IgE on sensitized cells
    • causes degranulation
  • Pharmacologically active mediators released exert biological effects on tissue
Most IgE reactions are mounted as a defense to parasitic infections
  • People with atopic tendencies cannot regulate IgE production
  • Remember that allergens are non-parasitic antigens that stimulate a type I hypersensitive response
Most allergic IgE responses occur on mucous membrane surfaces
  • Enter the body either by inhalation or ingestion
  • Common allergens are rye grass pollen, ragweed pollen, codfish, birch pollen and bee venom
    • ragweed pollen in a big problem in the U.S.
  • No single characteristic is common to all allergens
primary mediators of type i
Primary mediators of type I
  • Histamine
    • increases vascular permeability
    • smooth muscle contraction
  • Serotonin
    • same as histamine
  • Neutrophil chemotactic factor
    • neutrophil chemotaxis
  • Eosinophil chemotactic factor
    • eosinophil chemotaxis
  • Proteases
    • variety of effects
secondary mediators of type i
Secondary mediators of type I
  • Platelet-activating factor
  • Leukotrines (SRS-A)
  • Prostaglandins
  • Bradykinin
  • Cytokines
Type II hypersensitivity involves antibody destruction of cells
  • Best characterized by blood transfusion reactions
    • complement activated
  • Cell destruction can also occur through ADCC
  • Hemolytic disease of the newborn is another example
    • maternal IgG antibodies cross the placenta and destroy fetal red blood cells
Type III hypersensitivities are immune complex-mediated
  • When antigen reacts with antibody, an immune complex results
  • usually this helps clear the complex
  • Sometimes the complexes lead to tissue damage
    • depends upon quantity of complexes
    • also distribution in the body
  • Arthus reaction is where complexes are deposited near the site of antigen entrance
TDTH-mediated type IV hypersensitivity results from sensitization of TDTH cells
  • Several cytokines are secreted
    • IL-2
    • IFN-g
    • MIF
    • TNF-b
  • Cytokines attract macrophages which destroy innocent tissue
  • Reactions typically take 48-72 hours to develop
    • called delayed type hypersensitivity reactions
An example of a type IV reaction is the rash of poison ivy
  • Caused by a T cell response to a chemical in the plant
    • pentadecacatechol
  • Binds covalently to the host proteins
  • Result is a modified self protein that is recognized by CD4 T cells
  • These produce extensive inflammation