Exam 10: Chapter 14 (Allergies) Flashcards

1
Q

What are the properties of eosinophils?

A
  1. Present in the connective tissue underlying the epithelium
  2. Activated by external signals to release their granules
  3. Synthesize and secrete cytokines and lipid mediators after releasing their granules
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2
Q

What does the production of IgE rely on?

A

TH2 cells, which make IL-4, the substance that promotes class switching to IgE

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3
Q

What are the properties of allergens?

A
  1. Have to activate TH2 responses (must be proteins)
  2. Must be small enough to spread through air
  3. Must be stable and soluble
  4. Many are proteases
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4
Q

What are the immune system reactants for Type IV hypersensitivity?

A

TH1 cells, TH2 cells, and CTL

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5
Q

What can Type III hypersensitivity inflammation lead to?

A

Clotting and hemorrhage of the skin

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6
Q

Why is it important that mast cell activation is localized?

A

Effects of degranulation and secretion of inflammatory modulators on other tissues is minimized

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7
Q

What happens if allergic asthma progresses to chronic asthma?

A

Specific allergens are no longer necessary to activate an asthma response

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8
Q

What is another term for Type IV hypersensitivity?

A

Delayed type hypersensitivity

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9
Q

What is required for the production of mast cells?

A

Cytokine Stem Cell Factor (SCF)

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10
Q

Why do multiple antigens have the ability to activate the same mast cell?

A

Mast cells contain IgE specific for a number of different antigens, any of which can activate the mast cell

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11
Q

What is angioedema?

A

Diffuse swelling due to the activation of mast cells in the deeper layers of skin

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12
Q

How do basophils function?

A

Once activated by IgE, they release inflammatory mediators similar to mast cells

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13
Q

What causes Type IV hypersensitivity?

A

Antigen specific effector T cells

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14
Q

What is the consequence of activating the parasite response in the case of allergies?

A

Damage to normal tissues

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15
Q

What sort of reactions are caused by food allergens?

A

Smooth muscle contractions in the gut, urticaria and angioedema due to absorption of allergen into the blood

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16
Q

What is the role of TNF-alpha?

A

To work in concert with histamine to promote inflammation

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17
Q

What are the two roles of histamine?

A
  1. To act on endothelial cells to increase vascular permeability
  2. To act on smooth muscle cells, causing them to contract
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18
Q

How are basophil and eosinophil production related?

A

They are inversely proportional (increased production of one decreases production of the other)

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19
Q

What is required in order to elicit a Type I hypersensitivity response?

A

Prior exposure to the antigen that induces an IgE response

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20
Q

What must occur in order to get activation of the signaling pathway in Type I hypersensitivity?

A

Cross-linking of the FCeRI receptors for IgE

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21
Q

What immunoglobulin class mediates Type II hypersensitivity responses?

A

IgG

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22
Q

What is atopy?

A

A genetic predisposition to allergies

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23
Q

What is the late phase reaction?

A

Reaction that occurs hours after the immediate reaction and can last for hours. Caused by production of cytokines, leukotrienes, and chemokines by activated mast cells

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24
Q

What are some of the results of Type II hypersensitivity?

A

Patients can develop hemolytic anemia caused by RBC destruction, or thrombocytopenia caused by platelet destruction

25
Q

What other molecules are released by mast cells, besides histamine?

A
  1. TNF-alpha
  2. Proteases
  3. Cytokines
  4. Lipid mediators
26
Q

What causes Type III hypersensitivity?

A

Small immune complexes that get lodged in the lungs or blood vessels. Complement is fixed to these immune complexes and inflammation is induced, causing tissue damage

27
Q

How do inhaled allergens cause hay fever/allergic rhinitis?

A

By diffusing across the mucosa of the nasal passages and activating mast cells

28
Q

What is an example of a Type II hypersensitivity?

A

Penicillin

29
Q

What protease is present in connective tissue mast cell granules?

A

Chymotryptase

30
Q

How can drugs cause Type II hypersensitivity?

A

The drugs alter epitopes on cells so that the immune system generates IgM and IgG antibodies against these epitopes

31
Q

What are examples of Type IV hypersensitivity?

A

TB test, poison ivy

32
Q

Why are small immune complexes able to cause Type III hypersensitivity?

A

These small complexes are not cleared from circulation, but instead become deposited on the walls of vessels where they fix complement and induce inflammation

33
Q

What leads to anaphylactic shock?

A

Wide spread inflammation that causes vascular permeability, smooth muscle contraction, and loss of fluid from the blood

34
Q

What determines the granule contents of a mast cell?

A

The tissue of residence for the mast cell

35
Q

How does allergic asthma occur?

A

Inhaled allergens activate mast cells in the lungs, causing them to constrict and fill with mucus

36
Q

What is histamine?

A

One of the principle inflammatory mediators released by mast cells

37
Q

How are allergies treated?

A
  1. Allergens are avoided
  2. Antihistamines are used to block mast cells and their mediators
  3. Densensitization
38
Q

How does Stem Cell Factor (SCF) signal?

A

Through its receptor KIT, or CD117

39
Q

What causes Type II hypersensitivity?

A

Small molecules that alter the surface of human cells, making them antigenic

40
Q

What is the immediate reaction?

A

A reaction that occurs within minutes and lasts about 30 minutes. Referred to as wheal and flare. Caused by immediate degranulation

41
Q

What are the two distinct phases of IgE mediated allergic reactions?

A

An immediate reaction and a late phase reaction

42
Q

How is eosinophil activation regulated?

A
  1. Production of eosinophils requires IL-5, which is only produced by TH2 in response to infection
  2. Production of the chemokines that recruit eosinophils is limited to times of infection
  3. Resting eosinophils do not express FCeRI unless activated by inflammation
43
Q

What is another term for Type I hypersensitivity?

A

Immediate hypersensitivity

44
Q

What causes Type I hypersensitivity?

A

IgE activating the FCeR on mast cells, eosinophils, and basophils

45
Q

Why do Type IV hypersensitivities take a few days to occur?

A

The T cell response to the antigen must first be initiated, which takes a few days to happen

46
Q

Why are activated mast cells, eosinophils, and basophils able to amplify the IgE response?

A

These cells make CD40 ligand, which stimulates the B cells making IgE

47
Q

How does epinephrin counter anaphylaxsis?

A

By re-establishing the tight junctions between endothelial cells

48
Q

What is observed effect of histamine causing muscle contractions?

A

Airways constrict and mucus production increases

49
Q

What is an example of a Type I hypersensitivity?

A

Sensitivity to ragweed

50
Q

What protease is present in mucosal mast cell granules?

A

Tryptase

51
Q

What are the different common sources of allergens?

A

Inhaled materials, injected materials, ingested materials, contacted materials

52
Q

What is the role of lipid mediators?

A

Lipid mediators are inflammatory mediators that function similarly to histamine but are way more powerful

53
Q

What is systemic anaphalaxsis?

A

A systemic wide activation of mast cells due to an allergen reaching the blood stream

54
Q

What is the immune reactant for Type III hypersensitivity?

A

IgG

55
Q

What is the consequence of activating FCeRI?

A

The immediate release of preformed granules that contain inflammatory mediators

56
Q

What is the main function of mast cells?

A

To fight parasitic infections

57
Q

Why is an increase in FCgR expression beneficial for eosinophils?

A

It improves their ability to kill pathogens

58
Q

What is the role of cytokines?

A

IL-4 and chemokines attract other inflammatory cells