Immunology Chapter 17

1. 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

2. 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

3. 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

4. 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

5. 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

6. 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

7. 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

8. Secondary mediators of type I • Platelet-activating factor • Leukotrines (SRS-A) • Prostaglandins • Bradykinin • Cytokines

11. Patch test

12. 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

13. 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

14. Serum sickness is a classic example of an immune complex-mediated syndrome

15. 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

16. 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