Hypersensitivity Type I Flashcards

1
Q

type I hyper. is mediated by?

A

IgE mediated opsonization
(Anaphylactic and Atopic)

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2
Q

Type II Hyper. is mediated by?

A

IgM/IgG - mediated Opsonization
(Abs mediated)

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3
Q

Type III hyper. is mediated by?

A

Immune complex

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4
Q

Type IV HYper. is mediated by?

A

T-cells

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5
Q

Which hypersensitivity type is not Abs Mediated?

A

Type IV

* type I, II, III are all abs mediated

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6
Q

What triggers Type I hyper.

A

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

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7
Q

Treatment for Type I hypersensitivity caused by Systemic anaphylaxis (e.g. seafood, bee sting allergy)?

A

Epinephrine
(rapidly reverses the action of histamine on smooth muscle contraction and capillary dilation)

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8
Q

What triggers Type II hyper.

A

Abs bind to cell-surface antigens –> cellular destruction, inflammation, and cellular dyfunction

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9
Q

Examples of type II hypersensitivity

A
  1. Transfusion reactions
  2. Hemolytic disease of the newborn
  3. Drug-induced hemolytic anemia
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10
Q

The 2 phases of Type 1 Hyper.

A

1)Immediate - minutes
2)Delayed -hours

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11
Q

Explain the Immediate phase of type 1 hyper. upon contact with allergen

A

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

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12
Q

Explain what happens in the Delayed phase of Type I hyper.

A

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

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13
Q

Sensitization in type I hypersensitivity involves Class switcing to ———- production on first contact to Allergen

A

IgE

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14
Q

Explain how Sensitization occurs on first contact w/allergen in type I hyper.

A

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)
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15
Q

Fxn of Interleukin-4 (IL-4)?

A

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

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16
Q

Effector cells involved in type I hyper.?

A

mast cells, eosinophills and basophils

17
Q

Which Interleukins promote IgE production by B-cells?

A

IL-4 , IL-13

18
Q

Test used to detect allergic specific IgE in type I hypersensitivity

A

Skin test (wheal and flare response- takes min)

19
Q

Mucosal tissues are more prone to producing ——- responses

A

TH2

20
Q

what is responsible for the CM of Type I hyper?

* CM: clinical manifestations

A

Histamins, Tryptase and Leukotriens
(which are released in response to FcεRI cross-linking)

21
Q

first cells that respond to allergens?

A

Mast cells

* histamine is released within min of mast-cell activation

22
Q

fxn of Histamine?

A

1) Vasodilation
2) Increased mucous secretion
3) increased vascular permeability
4) Contraction of GI and bronchial SM

23
Q

Primary and secondary mediators released in response to cross-linking IgE-FcεRs by allergen on mast cell, eosinophils nad basophils

* type I Hypersensitivity

A
  • Primary–> histamins, tyrptase and heparin (inflammatory cytokines)
  • Secondary mediators –> Conversion of arachidonic acid into prostoglandins and leukotrines (inflammatory mediators)
24
Q

which mediators are responsible for the major cause of asthma sysmptoms?

A

Leukotrienes (LTC4, LTD4,LTE4) and prostoglandins (PGC2, PGE2)

25
Q

cytokine that recruits and activates eosinophils

A

IL-5

26
Q

Cytokine that stimultes Th2 responses to increase IgE production by B cells?

A

IL-4, IL-13

27
Q

Cytokine that attracts neutophils and other immune cells to the site of hypersensitivty (chemotactic factor)?

A

IL-8

28
Q

Cytokine that contributes to shock/ sepsis in systemic anaphylaxis

A

TNFα

29
Q

The consequences of IgE-mediated mast cell activation depend on the dose of antigen and its ———- of entry

A

Route of entry (GI, blood vessels, eyes, nasal passage)

30
Q

*Hyygeine hypothesis

Exposure to pathogens early in life provides a better T-cell balance and avoids dominance of ———- , which promotes ————— production by B cells

A

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

31
Q

How does Desensetization treat Type I hyper?

A

↓IgE, ↓ TH2, ↑IgG, ↑ regulatory T-cells and their cytokines