Types of hypersensitivity diseases

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Presentation transcript:

Types of hypersensitivity diseases The type of immune response and immunologic mechanisms that causes tissue injury The nature and location of the antigen that is the target of this response.

Types of hypersensitivity diseases Immediate H.S (Type I) caused by IgE Type II H.S caused by antibodies other than IgE can cause tissue injury and interfering with normal cellular functions. Type III H.S caused by deposition of circulating Immune complexes in tissues Type IV or Delayed type hypersensitivity caused by T cells and Macrophages

Disease caused by Immune responses *Activation of Th2 cells and production of IgE *Allergen Activation of Th2 B cell activation IgE binding of IgE to Fc receptor reexposure to Allergen release of mediators pathologic reactions

General features (1)

Immediate hypersensitivity با ورود آلرژن ، سلولهای B آن راشناسایی وپس از فعال شدن ، آنتی بادی IgE ترشح میکنند .

General features(2) There is a strong genetic predisposition for the development of immediate hypersensitivity *high level of IgE synthesis often run in families Class –II MHC alleles One locus for atopy is on chromosome 5,near the site of gene cluster encoding the IL-3,IL-4, IL-5,IL-9,IL-13 and IL-4R

General features افراد آتوپيك يا آلرژيك در مقابل عوامل آنتي ژنيك شايع محيطي ،پروتئين هاي موجود در گرده گياهان(pollen) ، مواد غذايي ، فضولات حيواني، سم حشرات يا برخي داروها از طريق Th2 پاسخ ميدهند آلرژنها پروتئينهاي ريز مولكول با حلاليت بالا ايمني ذاتي را فعال نمي كنند فراواني در محيط وبرخورد مكرر گليكوزيلاسيون بالا

َAllergens Type I is dependent on the activation of Th2 cells The clinical and pathologic manifestations of Type I:increased vascular permeability,vasodilation,smooth muscle contraction,local inflammation

Mast cell activation

Eosinophil and Basophil اين سلولها داراي گيرنده هاي high affinity براي IgE بنام FCR مي باشند گرانولهايي سيتوپلاسمي كه حاوي آنزيم ها و ساير مدياتورهاي فارماكولوژيك

Mast cell activation Rapid release of granule contents(degranulation)such as Histamine,tryptase,chymase,proteoglycans(heparin and chondroitin sulfate) Synthesis and secretion of lipid mediators(prostaglandines ,Leukotrienes) Synthesis and secretion of cytokines(IL-3,4,5,6,TNF-)

Mediators actions Histamine= bronchoconstrictor,vascular leak,intestinal hypermotility PGD2=vasodilator and bronchoconstrictor , neut. Chemotaxis LTC4=bronchoconstriction,inflammation PAF=bronchoconstriction ,vasodilator, inflammation

‍‍Clinical and pathologic features Hay fever(allergic rhinitis) Increased peristalsis Bronchial asthma Anaphylaxis

Wheal and Flare reaction

Therapy Inhibiting mast cell degranulation Antagonizing the effects of mediators Reducing inflammation Desensitization

Anti IgE as a therapy

Drugs Cromolyn sodium Theophyllin blocks phosphodiesterase epinephrin

Prick test

Prick test