Hypersensitivity Type I Flashcards
type I hyper. is mediated by?
IgE mediated opsonization
(Anaphylactic and Atopic)
Type II Hyper. is mediated by?
IgM/IgG - mediated Opsonization
(Abs mediated)
Type III hyper. is mediated by?
Immune complex
Type IV HYper. is mediated by?
T-cells
Which hypersensitivity type is not Abs Mediated?
Type IV
* type I, II, III are all abs mediated
What triggers Type I hyper.
1) Systemic Anaphylaxis (e.g. penicillin, seafood, drugs or bee sting allergies)
2) Localized Hypersensitivity rxn (e.g. Allergic rhinitis (hay fever), asthma, atopic dermatitis (eczema), food allergies)
*Anaphylactic and Atopic
Treatment for Type I hypersensitivity caused by Systemic anaphylaxis (e.g. seafood, bee sting allergy)?
Epinephrine
(rapidly reverses the action of histamine on smooth muscle contraction and capillary dilation)
What triggers Type II hyper.
Abs bind to cell-surface antigens –> cellular destruction, inflammation, and cellular dyfunction
Examples of type II hypersensitivity
- Transfusion reactions
- Hemolytic disease of the newborn
- Drug-induced hemolytic anemia
The 2 phases of Type 1 Hyper.
1)Immediate - minutes
2)Delayed -hours
Explain the Immediate phase of type 1 hyper. upon contact with allergen
Immediate (min) : Antigen crosslinks preformed IgE on presensitized mast cells –> immediate degranulation –> release of histamins (vasoactive amine), Tryptase (marker of mast cell activation), and leukotrienes
Explain what happens in the Delayed phase of Type I hyper.
late (hrs) : chemokines and cytokines (IL-4, IL-5, IL-8, IL-9,IL-3, GM-CSF, TNFα) –> attract inflammatory cells (e.g. eosinophils) and other mediators from mast cells –> inflammation and tissue damage
Sensitization in type I hypersensitivity involves Class switcing to ———- production on first contact to Allergen
IgE
Explain how Sensitization occurs on first contact w/allergen in type I hyper.
Upon first exposure to allergen -> Activation of TH2 (T-helper 2 cells) cells –> Promots the growth of B-cells –> Enhances Class switching to IgE through IL-4 production
- NOTE: mast cells express high levels of FcεRI, which mediate the response to allergens (Causing degranualtion)
Fxn of Interleukin-4 (IL-4)?
induces the diffrentiation of T cells to TH2 cells –> promote the growth of B-cells -> Enhances class switching to IgE
* Part of Type I hypersensitivity
Effector cells involved in type I hyper.?
mast cells, eosinophills and basophils
Which Interleukins promote IgE production by B-cells?
IL-4 , IL-13
Test used to detect allergic specific IgE in type I hypersensitivity
Skin test (wheal and flare response- takes min)
Mucosal tissues are more prone to producing ——- responses
TH2
what is responsible for the CM of Type I hyper?
* CM: clinical manifestations
Histamins, Tryptase and Leukotriens
(which are released in response to FcεRI cross-linking)
first cells that respond to allergens?
Mast cells
* histamine is released within min of mast-cell activation
fxn of Histamine?
1) Vasodilation
2) Increased mucous secretion
3) increased vascular permeability
4) Contraction of GI and bronchial SM
Primary and secondary mediators released in response to cross-linking IgE-FcεRs by allergen on mast cell, eosinophils nad basophils
* type I Hypersensitivity
- Primary–> histamins, tyrptase and heparin (inflammatory cytokines)
- Secondary mediators –> Conversion of arachidonic acid into prostoglandins and leukotrines (inflammatory mediators)
which mediators are responsible for the major cause of asthma sysmptoms?
Leukotrienes (LTC4, LTD4,LTE4) and prostoglandins (PGC2, PGE2)
cytokine that recruits and activates eosinophils
IL-5
Cytokine that stimultes Th2 responses to increase IgE production by B cells?
IL-4, IL-13
Cytokine that attracts neutophils and other immune cells to the site of hypersensitivty (chemotactic factor)?
IL-8
Cytokine that contributes to shock/ sepsis in systemic anaphylaxis
TNFα
The consequences of IgE-mediated mast cell activation depend on the dose of antigen and its ———- of entry
Route of entry (GI, blood vessels, eyes, nasal passage)
*Hyygeine hypothesis
Exposure to pathogens early in life provides a better T-cell balance and avoids dominance of ———- , which promotes ————— production by B cells
Th2, IgE
* IgE stimulates allergic response
* If we have low TH2 then we have TH1 cell dominance (when one increases the other decreases and vice verca)
* Hygeine hypothesis invloves TH1 cell dominance
How does Desensetization treat Type I hyper?
↓IgE, ↓ TH2, ↑IgG, ↑ regulatory T-cells and their cytokines
