Hypersensitivity Overview Flashcards

1
Q

This type of hypersensitivity reaction is IgE mediated and has 3 phases

A

Type I - Allergy/anaphylaxis/atopy

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2
Q

What characteristics are common to all hypersensitivity reactions? (3)

A

Adaptive immune response
Sensitization to antigen (primary response)
Secondary response (able to persist for years)

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3
Q

What are the 3 phases of an allergic reaction?

A

Sensitization phase: allergen specific IgE made which bind to receptors on mast cells and basophils
Activation phase: re-exposure to allergen IgE binding to its receptors —> inflammatory mediators
Effector phase: response to inflammatory mediators and clinical manifestations

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4
Q

What is the receptor to with IgE binds called?

A

FcR1

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5
Q

Where does the primary response in sensitization take place?

A

Lymphoid tissue

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6
Q

Response of this T-cell group is favoured in the sensitization stage

A

TH2 - subgroup of CD4 cells (helper)

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7
Q

What cytokines are made by TH2 cells in the sensitization stage?

A

IL4 - B cell switching to make IgE
IL13 - mucous production and smooth muscle contraction

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8
Q

What starts off the activation phase of a type I hypersensitivity reaction?

A

Antigen must cross link with IgE already bound to mast cell
Cross link = bind with 2 IgE on the same cell

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9
Q

What events take place in the activation phase of a type I hypersensitivity reaction?

A

Receptor aggregation (FcR1) and membrane fluidity changes
Increase in cAMP and Ca+
Degranulation

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10
Q

What events take place in the immediate part of the effector phase of type I hypersensitivity reaction?

A

Increased release of pro-inflammatory, pre-formed mediators
Synthesis of leukotrienes (lipid based inflammatory mediators)
Clinical manifestations: reps, skin, systemic
Consequence of inflammatory mediators
Happens within minutes of allergen exposure

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11
Q

What events take place in the late part of the effector phase of type I hypersensitivity reaction?

A

Caused by release of leukotrienes, chemokines, and cytokines
Pro-inflammatory chemical release —> other leukocyte recruitment to site of inflammation
Associted with sustained edema

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12
Q

These 3 mechanisms are involved in type II hypersentitivity reactions

A

Complement mediated reactions
Antibody dependent cell mediated cytotoxicity
stimulatory anti-receptor antibodies

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13
Q

What antibodies are involved in type II hypersensitivity reactions?

A
  • IgG or IgM
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14
Q

This hypersensitivity reaction involves antibody binding to a cell or tissue

A

Type II

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15
Q

Give me some examples of type II hypersensitivity reactions

A

Transfusion reaction
Hemolytic disease of the newborn

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16
Q

Interaction with this substance can cause type I, II, or III reaction depending on the type of antigenic modulation and the antibody

A

Drug interactions

17
Q

What is the mechanism of type III hypersensitivity reactions?

A

Immune complex formation and deposition in tissue
Complement and inflammatory response
Effector cell activation esp neutrophils

18
Q

What normally happens to immune complexes?

A
  • Soluble complexes —> complement activation —> C3b deposition —> CR1 binding them and taking them to the liver and spleen for clearance
19
Q

What kind of antigens are involved in type III hypersensitivity?

A

Endogenous or exogenous

20
Q

Give examples of type III reactions

A

Serum sickness
Complement deficiency
Autoimmune diseases ex lupus

21
Q

What is the other name for type IV hypersentitivity reasons?

A

Delayed type hypersensitivity reactions

22
Q

This hypersensitivity is T cell mediated rather than antibody mediated

A

Type IV aka delayed type hyerpsensitivity reaction

23
Q

What are the phases in type IV reactions?

A

Sensitization: MHC class II and dendritic cells, T cell activation. Takes 1-2wks to dev
Elicitation: Re-exposure to sensitized antigen —> T1H memory cell activation, chemokine and cytokine production; recruitment of macrophages into tissue