Hypersensitivity type I
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Transcript Hypersensitivity type I
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 IgEترشح
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 آتوپیك یا آلرژیك در مقابل عوامل آنتي ژنیك شایع
محیطي ،پروتئین هاي موجود در گرده گیاهان)(pollen
،مواد غذایي ،فضوالت حیواني ،سم حشرات یا برخي
داروها از طریق Th2پاسخ میدهند
آلرژنها پروتئینهاي ریز مولكول با حاللیت باال
ایمني ذاتي را فعال نمي كنند
فراواني در محیط وبرخورد مكرر
گلیكوزیالسیون باال
َ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
affinityبراي IgEبنام FCR
مي باشند
گرانولهايي سيتوپالسمي كه حاوي آنزيم
ها و ساير مدياتورهاي فارماكولوژيك
Mast cell activation
Rapid release of granule
contents(degranulation)such as
Histamine,tryptase,chymase,proteoglyca
ns(heparin and chondroitin sulfate)
Synthesis and secretion of lipid
mediators(prostaglandines ,Leukotrienes)
Synthesis and secretion of cytokines(IL3,4,5,6,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