1. L ECTURES 2014 KEFAH F. HASSOON L ECTURE N O. 1 Immune System Disorders Auto-immune Diseases Hypersensitivity reactions

2. H YPERSENSITIVITY REACTIONS The immune system is an integral part of human protection against disease, but the normally protective immune mechanisms can sometimes cause detrimental reactions in the host. A subsequent exposure to the same antigens may cause hypersensitivity reactions.

3. Hypersensitivity reactions can be divided into four types ( by R. Coombs and P. Gell) based on the mechanisms involved and time taken for the reaction : type I, type II, type III and type IV.

4. TYPE I HYPERSENSITIVITY is also known as: Immediate – Type Hypersensitivity OR Anaphylactic Hypersensitivity OR Allergy. Characters The reaction may cause a range of symptoms from minor to death (Systemic &regional dysfunction ). The reaction usually takes 15 - 30 minutes from the time of exposure to the antigen(Quickly onset), or sometimes it may have a delayed onset (10 - 12 hours).

5. C HARACTERS Antigens that induce formation of antibodies is called Allergens. Mediated by IgE. parasitic infection & non- parasitic infection Genetic predisposing. ( Atopy ： the genetic predisposition to synthesize primate levels of IgE specific for external allergens ).

6. T HE MECHANISM OF REACTION A subsequent exposure to the same allergen cross links the cell-bound IgE and triggers the release of various active substances (mediators). ++ ++ Mast cell degranulation is preceded by increased Ca ++ influx, which is a crucial process, to increase cytoplasmic Ca ++ than promote degranulation.

7. The primary cellular component in this hypersensitivity is the mast cell or basophil (mainly) than platelets, neutrophils and eosinophils. High affinity receptor of the IgE on mast cell and basophil,Eosinophil ( Fc  RII), while the Fc  RI (low affinity ).

9. Biological Mediators: Histamine & Serotonin: Dilates and increases permeability of blood vessels (swelling and redness), increases mucus secretion (runny nose), smooth muscle contraction (bronchi). Prostaglandins: Contraction of smooth muscle of respiratory system and increased mucus secretion. Leukotrienes: Bronchial spasms.

10. Mediators: The reaction is amplified by PAF (platelet activation factor) which causes platelet aggregation and release of histamine &heparin. Eosinophil chemotactic factor (ECF) And Neutrophil chemotactic factors (NCF) attract eosinophils and neutrophils, respectively, which release various hydrolytic enzymes that cause necrosis.

11. C OMMON ALLERGIN IN TYPE I Protein (vaccine,&Infection like bacteria and virus) Plant (Rye grass) Drugs ( Penicillin, Sulfonamides, local anesthetics, Aspirin, salicylates, morphine, x-ray dye ) Insects products ( bee venom,ant venom, mites,cockroach) Mold spores Animals hairs and latex) Foods( nuts, milk, peas, eggs, seafood, Crab, shrimp, potato, tuna )

12. B IOLOGICAL EFFECTORS  Skin allergy (hives and eczema)  Respiratory allergic diseases rhinitis, bronchopulmonary tissues (asthma)  Gastrointestinal allergic diseases Gastroenteritis  Anaphylaxis

13. A NAPHYLACTIC SHOCK  Anaphylaxis is a severe.  whole-body allergic reaction.  a life-threatening.  can occur at any time &  Risks include a history of any type of allergic reaction.

14. Systemic (Anaphylaxis shock) Symptoms include: drop in blood pressure, smooth muscle contraction, bronchiole constriction (suffocation). Localized Examples: Hay fever (allergic rhinitis), asthma,food allergies, atopic dermatitis (eczema)

15. D IAGNOSIS : skin (prick and intradermal) tests, measurement of total IgE and specific IgE antibodies against the suspected allergens. Enzyme Immuno Assay (EIA). There appears to be a genetic predisposition for atopic diseases and there is evidence for HLA (A2) association.

16. I NTRADERMAL TEST.