hypersensitivity type 1 and 2

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hypersensitivity type 1 and 2
2013-08-05 14:29:35

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  1. Hypersensitivity reactions: is it chronic or acute pathology?
  2. hypersensitivity rxn involve what
    IgG or specific T cell
  3. type I hypersensitivity
    anaphylactic type (allergy and anaphyxasic) 

  4. type II hypersensivity
    AB dependent (AB to fixed tissue antigen)
  5. type III hypersensitivity
    immune complex-mediated
  6. type IV hypersensitivty
    celled-mediated (delayed)
  7. type I - mechanism
    • 1.Allergen cross-links IgE antibody to activate mast cells and Basophils
    • –Initial response (5 to 30 minutes)

    • 2.Release of vasoactive amines & other mediators from basophils and mast cells
    • –Late-phase reaction (2 to 8 hours & lasts for days)

    3.Recruitment of other inflammatory cells

    4.Mucosal epithelial cell damage
  8. true or false:
    Type I hypersensitivity requires a “primed” immune system
  9. Type I hypersensitivity is quality and location dependent
  10. activating mast cell
    C3a and C5a

    IgE on mastcell
  11. Initial phase - type I
    One of the key immediate mediators is histamine. It causes a rapid increase in vascular permeability as well as contraction of smooth muscle.

    Histamine ↑ vascular permeability vasodilation bronchoconstriction mucus production
  12. key mediator in initial phase of Type I
  13. beside histamine, what else is produce in initial phase?
    • protease (tryptase)
    • chemotactic factors (eosinophil and neutrophil)
  14. Late phase - type I produces what molecule
    cytokine: TNf a, IL-1, IL-4, IL-5, IL-6 --> recruit and activate many types inflammatory cells 

    • Leukotrienes:
    • C4&D4 - asoconstriction
    • B4 - chemotactic: Eosinophil, neutrophil, monocytes & leukocyte adhesion

    Protaglandin D2: vasodilation, mucous secretion

    • Platelet-activating factor 
    • platelet aggregation
    • vasodilation
    • bronchoconstriction
    • 100x > histamine (inc vascular permeability, vasodilation)
    • chemotactic for eosinophil & neutrophils
  15. which phase is the major cause of symptoms in Type I hypersensitivity disorders?
    late phase
  16. timeline for type I hypersensitivity (early and late phase)
    • early phase: minutes
    • Late phase: hours-days
  17. Atopic asthma
    classic example of type I IgE mediated hypersensitivity.

    predisposition to develop localized immediate hypersensitivity reactions to a variety of inhaled and ingested allergens

    Atopic individuals tend to have higher serum IgE levels, more IL-4 producing TH2 cells, compared with the general population.  

    family history is common
  18. 2nd exposure of antigen to atopic asthma
    • releases mediators that open mucosal intercellular junctions > more antigen reaches mast cells
    • --> bronchoconstriction, edema, mucus secretion

    Late phase response: inflammatory cell recruited including eosinophils (amplify and sustain inflammatory response)
  19. airway remodeling from atopic asthma
    -Thickening of the basement membrane of the bronchial epithelium

    -Edema and an inflammatory infiltrate in the bronchial walls, with a  prominence of eosinophils and mast cells 

    An increase in the size of the submucosal glands

    Hypertrophy of the bronchial muscle walls
  20. Systemic analphylaxis
    •Urticaria (hives)

    •Pulmonary bronchoconstriction

    •Laryngeal edema

    •GI tract musculature over activity

    anaphylactic shock --> systemic vasodilation
  21. testing for systemic type I hypersensitivity
    injection and test and wheal and flare
  22. atopic asthma - clinical course
    • Asthmatic attack lasts up to several hours and causes recurrent episodes
    • Chest tightness, breathlessness, wheezing
    • Cough without sputum
    • Difficulty exhaling (air is trapped distal to bronchi)

    • Asthma attack due to
    • Intermittent and reversible airway obstruction

    Chronic bronchial inflammation with eosinophils

    Bronchial smooth muscle cell hypertrophy and hyper-reactivity (bronchoconstriction)
  23. type II HS - diseases
    • -Normal cell surface molecule
    • Goodpasture’s Disease – anti-glomerular
    • basement membrane protein
    • Graves Disease (hyperthroidism):  Ab
    • mediated TSH stimulation

    • -Adsorbed exogenous antigens (Drug or metabolite)
    • Hemolytic anemia or thrombocytopenia
  24. Goodpasture Disease
    • •is an autoimmune disease in which kidney and lung injury is caused by circulating
    • autoantibodies against the basement membrane type IV collagen.

    •Teens-20’s; males mostly

    • •Initiate inflammatory destruction of the basement membrane in renal glomeruli and
    • pulmonary alveoli > proliferative and rapidly progressive glomerulonephritis and necrotizing hemorrhagic interstitial pneumonia

    Get nephritis and lung hemorrhage
  25. Mechanism for Antibody Mediated Injury
    Complement Dependent reactions

    Antibody-Mediated Cellular Dysfunction
  26. Complement-Dependent Reactions - type 2 HS
    –Direct cell lysis

    –Opsonization and Phagocytosis

    • Ab binding to Fc receptors on macrophages
    • as well as complement breakdown production induce inflammation.
  27. Complement-Dependent Reactions - type 2 HS
    • •Transfusion reactions
    • –Blood grp Ags

    • •Erytroblastosis fetalis (Immune Hydrops)
    • –Rh incompatibility
    • –ABO incompatibility

    •Autoimmune hemolytic anemia, autoimmune thrombocytopenic purpura

    • –Ab
    • produced against self-blood cells

    • •Drug reactions
    • –Penicillin adsorbed to cell surface

    • •Pemphigus vularis
    • –Abs against desmosomal
    • proteins that lead to disruption of epidermal intercellular junctions
  28. Pemphigus Vulgaris
    • •a blistering disorder caused by IgG antibodies directed against epidermal
    • cadherin (protein in intercellular junctions of epidermal cells)

    •Pemphigus vulgaris is most common type.  Lesions are first seen in oral and genital mucosa.

    Superficial blisters that rupture easily 

    • Ab disrupts intercellular adhesions,
    • leading to inflammation, leading to blisters.
  29. Bullous Pemphigoid
    •Similar to Pemphigus vulgaris but IgG antibodies disrupt the basal cell-basement membrane attachments (hemidesmosomes).

    •Blisters form that do not rupture easily.

    •Oral involvement is present in 1/3 of patients.

    •More common in elderly.
  30. Antibody-mediated cellular dysfunction
    • Myasthenia gravis 
    • grave disease

    Anti-receptor antibodies disturb the normal function of receptors.