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Immunology > Allergy, Hypersensitivity, and Chronic Inflammation > Flashcards

Allergy, Hypersensitivity, and Chronic Inflammation Flashcards

1
Q

Hypersensitivity definition

A

Failure of tolerance- inappropriate, vigorous innate and adaptive responses to antigen

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2
Q

Type 1 hypersensitivity: mediator and symptoms

A

IgE

Anaphylaxis, hay fever, asthma, hives, food allergies, eczema

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3
Q

Does an IgE response happen during a first or secondary exposure?

A

Secondary- first exposure doesn’t trigger reaction

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4
Q

Type of receptor that IgE acts upon

A

Fc eta receptors

Present on surfaces of immune cells

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5
Q

Two types of Fc eta receptors

A

High affinity: Fc eta R1

Low affinity: Fc eta R2

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6
Q

Differences between Fc eta R1 and Fc eta R2

A

Fc eta R1: responsible for most allergy symptoms, expressed by mast cells and basophils
Fc eta R2: regulates production of IgE by B cells

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7
Q

Result of binding to Fc eta R1

A

Degranulation and release

Formation and secretion of mediators such as histamine and cytokines

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8
Q

Type 1 hypersensitivity: early response

A

Occurs within minutes of allergen exposure

Mediated by mast cell granule release of histamine, leukotrienes, and prostaglandins

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9
Q

Type 1 hypersensitivity: late response

A

Hours after allergen exposure

Influx of neutrophils, eosinophils, and TH2 cells

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10
Q

Diagnosis of Type 1 reaction

A

Skin test: look for localized reaction to allergen

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11
Q

Treatment of type 1 hypersensitivity

A

Antihistamines
Leukotriene antagonist (targeting secondary mediator)
Steroids (asthma)
Immunotherapy: anti-IgE antibody

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12
Q

Hyposensitization

A

Treatment for type 1 hypersensitivity

Switching IgE response to IgG response by injecting small amounts of allergen

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13
Q

Hygiene hypothesis

A

Exposure to some pathogens early in life provides a better T-cell balance (less TH2, which promotes IgE production)
High incidence of allergy and asthma in developed countries, but lower in farm environment

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14
Q

Type 2 hypersensitivity: mediator

A

Antibodies (other than IgE) bind to antigens on person’s own cell surfaces

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15
Q

Antibody bound to cell surface antigen can induce cell death in what 3 ways?

A
  1. Complement activation/ MAC
  2. Cytotoxic cells bind to antibodies on target cell and promote killing
  3. Opsonization: mediate phagocytosis by phagocytes
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16
Q

Conditions in which type 2 hypersensitivities occur

A

Transfusion reactions: receiving infusion of non-matching blood type
Hemolytic disease of newborn: Rh negative mother mounts immune response against Rh positive fetus
Drug-induced hemolytic anemia: antibiotics such as penicillin, cephalosporin, and streptomycin attach to proteins on red blood cells, stimulating complement-mediated destruction

17
Q

Which types of hypersensitivities can penicillin induce?

A

All 4

18
Q

Type 3 hypersensitivity: mediator

A

Immune complexes: antigen/antibody complexes deposited in tissues induce complement activation and inflammation due to influx of neutrophils

19
Q

Symptoms of type 3 hypersensitivity

A

Fever, rashes, joint pain, lymph node enlargement

20
Q

Serum sickness

A

Type 3 hypersensitivity

Treatment with antibody serum can lead to systemic immune complexes against the treatment

21
Q

Arthus reaction

A

Type 3 hypersensitivity
Swelling and localized bleeding
Caused by injection of antigen in person with high levels of circulating antibody specific to it

22
Q

Type 4 hypersensitivity: mediator

A

T cells

23
Q

Type 4 hypersensitivity: mechanism

A

1st exposure produces memory T cells
2nd exposure produces effector cells
Effector cells release cytokines which activate macrophages and other inflammatory mediators

24
Q

Type 4 hypersensitivity: symptoms

A

Usually contact dermatitis

25
Q

Common inducers of type 4 hypersensitivity

A

Poison ivy
Solvents
Cosmetics (hair dyes)
Metals (Ni)

26
Q

Delayed type (type 4) hypersensitivity: TB test

A

Secondary exposure to sensitizing antigen

Prolonged inability to clear antigen: TB-positive individuals

Immunology (23 decks)

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