Immunology Chapter 17 Richard L. Myers, Ph.D. Department of Biology Southwest Missouri State Temple Hall 227 Telephone: Homepage: myersr/index.html TopClass:

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

T DTH -mediated type IV hypersensitivity results from sensitization of T DTH cells Several cytokines are secreted –IL-2 –IFN-  –MIF –TNF-  Cytokines attract macrophages which destroy innocent tissue Reactions typically take 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