Hypersensitivity reactions
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Hypersensitivity reactions. Type. Mechanism. Antigen. Onset. IgE-Ag triggers Mast cell mediators. Allergen minutes. I. IgG or IgM binds to cell surface; ADCC or complement. Cell surface molecule. Few hours. II. Immune complexes, inflammation. Soluble or particulate. Few

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Hypersensitivity reactions

Type

Mechanism

Antigen

Onset

IgE-Ag triggers

Mast cell mediators

Allergen minutes

I

IgG or IgM binds to

cell surface; ADCC

or complement

Cell surface

molecule

Few

hours

II

Immune complexes,

inflammation

Soluble or

particulate

Few

hours

III

Cytokines (T cells,

Macrophages, CTL)

Chemicals,

intracellular

1-3

days

IV



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Atopy- hereditary predisposition toward allergic

reactions

Mechanism not clear- may map to chromosomal

region encoding many cytokines

Tend to occur on mucous membranes- allergens

either inhaled or ingested



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IgE discovered by Ishizakas in 1960s-

normally very rare in serum

Larger molecule than IgG

Not stable in serum

Binds to receptors on basophils and mast cells;

then is stable for several weeks


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What are mast cells and basophils?

Basophil- rare blood cell

Mast cells- found in connective tissue

Granules contain active mediators

Also secrete lots of cytokines: IL-1, IL-4, IL-5, IL-6,

GM-CSF, etc.

Also have high- and low-affinity receptors for IgE


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Events in an allergic reaction

First exposure

B cells produce allergen-specific IgE

IgE reacts with Fc receptors on mast cells



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Early events required for degranulation

Histamine is preformed p. 369


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Histamine release occurs within minutes

Binds to receptors on target cells

smooth muscles contract

eosinophils attracted

mucus secretion

platelet activation

blood vessel dilation

Blocked by various compounds: antihistamines,

Epinephrine, corticosteroids



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Effects of type I reactions

Systemic anaphylaxis

Respiration becomes difficult

Blood pressure drops

Smooth muscles of bladder and GI tract

contract

Bronchoconstriction

Countered by epinephrine

relaxes smooth muscles

decreases vascular permeability

improves cardiac output


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Localized anaphylaxis

Allergic rhinitis (hay fever)- nasal mucosa

Asthma- lower respiratory tract

bronchoconstriction, edema, mucus,

inflammation



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Early response- histamine, leukotrienes,

prostaglandins

bronchoconstriction, vasodilation,

smooth muscle contraction

Late response- IL-4, TNF-, etc.

endothelial cell adhesion

Also leukocyte migration, leukocyte

activation factors

Neutrophils (also eosinophils) cause a lot of

tissue damage


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Food allergies

cells are sensitized in GI tract

if bloodborne, can cause symptoms

such as asthma or hives

Atopic dematitis (eczema)

Late-phase reactions (not asthmatic)

mast cells release cytokines

eosinophils, neutrophils recruited


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Regulation of type 1 hypersensitivity

Antigen stimulation

IL-4 induced class switch

TH2 cells, also mast cells

IFN- reduces IgE production


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Detection of type I hypersensitivity (p. 375)

RIST- total serum IgE

RAST- IgE specific for a single allergen

Skin test


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Therapies

Avoidance

Hyposensitization

Drugs

antihistamines (block receptors)

epinephrine (maintain high cAMP and prevent

degranulation

cromolyn sodium block calcium flux

and more (p. 377)


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Type II: antibody-mediated cytotoxic reactions

Antibodies bind to cells and mediate their

destruction

Transfusion reactions (ABO blood group Ags)

Drug-induced hemolytic anemia

drugs absorb to RBCs, like hapten-carrier


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p. 415

p. 380



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Type III: Immune complex disease

Sometimes antibody- (soluble) antigen complexes

are not cleared like they should be

When deposited in tissue, they cause damage

complement activation- produces

inflammatory mediators

neutrophils

Arthus reaction- sensitized person develops

a reaction at site of exposure (slower than

type I)



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Generalized reaction- large amounts of antigen

enter bloodstream

Immune complexes form

Serum sickness- immunization with foreign serum

Complexes tend to accumulate in kidneys,

arteries, joints

Autoimmune disease

Infectious disease (malaria, parasitic disease)

Cross-reactivity with bacterial or viral antigens



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Type IV (TDTH and TC, or delayed-type)

Can lead to granuloma formation

Detected with skin test (e.g., skin test for

tuberculosis)

Contact dermatitis- when small molecules

complex with skin proteins

Internalized and presented by Langerhans

cells

TH1 response; elicitation of macrophages


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Helps protect against intracellular pathogens

Granulomas form in chronic reactions

DTH response declines in immune deficient

people (with T cell deficiency)


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