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Type I HS (Anaphylactic type)

  1. Rapidly developing immunologic reaction occurring within minutes after the combination of an antigen with antibody bound to mast cell or basophils in individual previously sensitized to antigen.
  2. Systemic - hormones, antisera, drugs (penicillin)
  3. Local ( Atopy) - skin, allergy, hives
    1. Allergic Rhinitis                
    2. Allergic conjunctivitis
    3. Hay fever                 
    4. Bronchial Asthma         
    5. Allergic Gastroenteritis
Two phases:
  1. Initial Response:
    It is evident within 5-30 min Q, subsides in 60 min,
    1. Vasodilation                     
    2. Vascular leakage
    3. Smooth muscle spasm                      
    4. Glandular secretions
  2. 2nd late phase Reactions:
    1. More intense infiltration of tissues with neutrophils, eosinophils, basophils, monocytes, CD4 + T cells
    2. Sets in 2-8 hours Q
    3. Lasts for several days, Tissue destruction
    4. Mast cell & Basophils; Central to development of Type IHS
    5. Activated by cross linking of IgE Fc receptors
Other activators of mast cells Q
  1. C3a & C5a (Anaphylatoxins)
  2. Macrophages derived CKs (lL-8)
  3. Codeine, Morphine               
  4. Mellitin (Bee venom)            
  5. Physical Stimuli (heat cold, sunlight)
Fig: Pathogenesis of immediate (type I) hypersensitivity reaction. The late-phase reaction is dominated by leukocyte infiltration and tissue injury. TH2, T-helper type 2 CD4 cells.
Primary Mediators: Mediate initial response
  1. Biogenic Amines - Histamine        
    1. Smooth muscle contraction  
    2. Vascular permeability          
    3. Secretion
  2. Chemotactic mediators ­
    1. Eosinophil chemotactic factor
    2. Neutrophil chemotactic factor
  3. Enzymes- (In granule matrix cause tissue destruction, lead to generation of kinins and C3a.
    Pro teases (chymase, tryptase) & Acid hydrolases
  4. Proteoglycans Q
    1. Heparin                 
    2. Chondroitin sulfate
      They help to store mediators in the granules. 
Secondary Mediators: Responsible for late phase
  1. Lipid Mediators →
    1. Arachidonic acid pathway
    2. LTB4: chemotactic for neutrophils, eosinophils, monocytes
    3. LTC4 & LTD4: Vasoactive
    4. Spasmogenic
    5. PGD2- most common abundant mediator derived by COX pathway in mast cell
    6. Bronchospasm, ↑mucus secretion
    7. Platelet activating factor (PAF)
      • Causes platelet aggregation, histamine release, bronchospasm,
      • ↑Vascular permeability, vasodilation
      • Chemo tactic for neutrophils & eosinophils
  2. Cytokines
    1. TNFα, IL-l,
  • In late phase: Eosinophils are particularly important
  • Survival favoured by IL-3, IL-5, GM-CSF
  • Exotoxin & RANTES – Chemotaxis
Tab: Summary of the action of mast cell mediators in immediate (type I) hypersensitivity
Action Mediator
Vasodilation, increased vascular permeability Histamine, PAF, Leukotrienes C4, D4, E4, Neutral proteases that activate complement and kinins, Prostaglandin D2
Smooth muscle spasm Leukotrienes, C4, D4, E4, Histamine, Prostaglandins, PAF
Cellular infiltration Cytokines, eg., TNF, Leukotriene B4, Eosinophil and neutrophil chemotactic factors (not defined biochemically) PAF
  1. Local Anaphylaxis: Q
Atopy: Genetically determined predisposition to develop localized anaphylactic reactions to inhaled or ingested allergens.
Seen in 10% of population or Positive family h/o of allergy in 50%

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