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: rlm967f@mail.smsu.edu

• 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