Immunology Chapter 17 Richard L. Myers, Ph.D. Department of Biology Southwest Missouri State Temple...
-
Upload
emery-park -
Category
Documents
-
view
213 -
download
0
Transcript of Immunology Chapter 17 Richard L. Myers, Ph.D. Department of Biology Southwest Missouri State Temple...
ImmunologyChapter 17
• Richard L. Myers, Ph.D.
• Department of Biology
• Southwest Missouri State
• Temple Hall 227
• Telephone: 417-836-5307
• Email: [email protected]
• Homepage: http://creative.smsu.edu/biology/myersr/index.html
• TopClass: http://creative.smsu.edu
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
• 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• 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
• Platelet-activating factor
• Leukotrines (SRS-A)
• Prostaglandins
• Bradykinin
• Cytokines
Patch test
• 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
Serum sickness is a classic example of an immune complex-mediated syndrome
• TDTH-mediated type IV hypersensitivity results from sensitization of TDTH cells
• Several cytokines are secreted– IL-2– IFN-– MIF– TNF-
• 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