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Immunology: hypersensitivity, autoimmunity, immunodeficiency > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is a hypersensitivity?

A

Over reaction of the immune system to a harmless antigen (an antigen that most people don’t react to)

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2
Q

What is the distinguishing feature between the four types of hypersensitivity?

A

Whether the response is mediated by antibodies or cells

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3
Q

What are Type I immediate hypersensitivities more commonly called?

A

Allergies or atopic disorder

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4
Q

What immune molecule is responsible for Type I immediate hypersensitivities?

A

IgE

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5
Q

What does the severity of a Type I hypersensitivity depend on?

A

The route of entry taken by the antigen and the location of the responding cells

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6
Q

What makes someone genetically susceptible to having a type I immediate hypersensitivity?

A

High levels of IgE and eosinophils

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7
Q

What are the four main sources of allergens?

A

Inhaled materials, injected materials, ingested materials, contacted materials

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8
Q

What do all allergens have in common?

A

Low molecular weight, highly soluble particles, carried on proteins, contain peptides that can be presented to MHC Class II, effectively activate Th2

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9
Q

TH1 or TH2 are primarily responsible for type I immediate hypersensitivity?

A

TH2

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10
Q

What cytokine is responsible for stimulating IgE?

A

IL-4

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11
Q

How is the first exposure different from the second exposure for Type I hypersensitivities?

A 
First: no reaction; get sensitization to the allergen; TH2 cells stimulate class switching on B cells to IgE which bind to receptors on mast cells
Second: Crosslinking of IgE leads to degranulation of mast cells and get symptoms
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12
Q

What mechanism other than IgE crosslinking leads to degranulation of mast cells?

A

Crosslinking of IgG, C5a binding to complement receptors on mast cells

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13
Q

What is released from mast cells? How long after exposure do they show up?

A

Lipid mediators/vasoactive amines: leads to the immediate hypersensitivity reaction; minutes after exposure to Ag
Cytokines: leads to the late phase reaction; 2-4 hours after exposure to Ag

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14
Q

In a Type I hypersensitivity, how does the immediate phase differ from the late phase? What mediators are responsible for each?

A

Immediate: wheal and flare, from lipid mediators/vasoactive amines
Late: widespread inflammation, from cytokines

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15
Q

The wheal and flare are characteristic of which hypersensitivity? What causes the wheal and flare?

A

Type I immediate phase
Wheal- from leakage
Flare-from engorgement with RBC

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16
Q

What tissues are effected by lipid mediators? How are they effected?

A

Leaky vessels, bronchoconstriction, intestinal hypermotility, general inflammation

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17
Q

What were mast cells/eospinophils initially used for protection against?

A

Parasites

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18
Q

TNF leads to the expression of what when released from mast cells?

A

Adhesion molecules on endothelial cells

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19
Q

How are basophils/eosinophils activated?

A

By mast cell release

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20
Q

As the basophil population increases, what happens to the eosinophil population?

A

Decreases

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21
Q

During which part of the Type I hypersensitivity are eosinophils found?

A

Late phase

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22
Q

What are the main effects of eosinophils?

A

Promote chemotaxis, mucus production, and tissue repair

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23
Q

What is urticaria?

A

Localized swelling

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24
Q

What is angiodema?

A

Deep and diffuse swelling

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25
Q

What is the response to a subcutaneous allergen?

A

Second exposure leads to crosslinking of IgE causing mast cell degranulation and urticaria

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26
Q

When inhale an antigen, the antigen is presented to T cells leading to the secretion of which cytokine? (this cytokine is responsible for class switching to IgE)

A

IL-4

27
Q

Upon second exposure, where will an inhaled Ag activate mast cells? What will be the result?

A

Mucosa- results in blood vessel permeability and recruitment of eosinophils which release mucus

28
Q

What cytokine is responsible for allergic asthma? What type of hypersensitivity is allergic asthma considered?

A

IL-13; Type 1

29
Q

What happens during an acute asthmatic reaction?

A

Mucosal mast cells capture Ag and degranulate; leads to bronchoconstriction, increased mucus production, and increased vascular permeability

30
Q

What cells are responsible for chronic asthmatic reaction?

A

cytokines and eosinophil products

31
Q

What is the difference between an acute asthmatic reaction and a chronic asthmatic reaction?

A

Acute: the allergen is present and leads to degranulation of mast cells
Chronic: a trigger (temp/cold/smoke) causes symptoms even though the allergen isn’t present

32
Q

Ingestion of food allergens leads to diarrhea and vomiting; why does this happen?

A

Antigen can get into the blood stream and mast cell degranulation leads to smooth muscle contraction

33
Q

What is the most severe Type I hypersensitivity?

A

Systemic anaphylaxis

34
Q

What tissues can be effected by a systemic allergen?

A

Heart and vascular system, respiratory tract, GI tract

35
Q

Why are systemic allergens life threatening?

A

Swelling in the heart leads to irregular heartbeat/ drop in BP/ reduced oxygen disseminaton
Bronchoconstriction of airways leads to difficulty breathing
GI smooth muscle contracts: get vomiting and diarrhea

36
Q

How are systemic allergen responses treated?

A

Epinephrine

37
Q

What is the difference between an ingested allergen and a systemic allergen in terms of location of the mast cells?

A

Ingested: mast cells are in the mucosa and then the antigen can enter the bloodstream
Systemic: antigen is in the bloodstream and then enters tissues to activate mast cells all over the body

38
Q

Why do allergies tend to run in families?

A

There are certain genes that are associated with allergies

39
Q

If someone has more IL-4 will they be more or less susceptible to allergies?

A

More susceptible

40
Q

Developed countries have a higher incidence of allergies than poorer countries where still have exposure to parasites. What is considered protective against allergic responses?

A

A balance between TH1 and TH2 with a slight favoring for TH1

41
Q

If someone has a low genetic susceptibility to allergies and living in an unhygenic environment, will their immune system be pushed towards a TH1 or TH2 response?

A

TH1

42
Q

What are some potential treatments for Type I hypersensitivities?

A

Avoid allergen, treat symptoms (anti-histamines, corticosteroids, aluterol, epinephrine), try desensitization, block cytokines

43
Q

How does desensitization work?

A

Expose to small amounts of antigen to try and get more IgA and IgG Ab which then block the binding of Ag from binding to IgE on mast cells

44
Q

What types of hypersensitivties are important for autoimmunity diseases?

A

Types 2, 3, 4

45
Q

What immune molecule mediates Type II?

A

IgG and complement

46
Q

How can penicillin lead to a type II hypersensitivity?

A

Alters the proteins on RBC so that they look foreign; IgG binds and binds complement resulting in lysis of the RBC

47
Q

Why are we only tolerized to our own blood antigens?

A

Blood antigens are similar to bacterial antigens so don’t want to limit are immune response and the ability

48
Q

Which blood type is the universal donor?

A

O

49
Q

Which blood type is the universal recipient?

A

AB

50
Q

Which immune cells are responsible for Type III hypersensitivities?

A

Large Ag:Ab complexes that can’t be cleared by complement

51
Q

Why are Ag:Ab complexes a problem?

A

Deposited systemically and can result in tissue damage

52
Q

When Ag:Ab complexes are deposited in the blood vessel walls, renal glomeruli, and joint spaces, what types of disease result? How do the reactions that induce these reactions get into the body?

A

Vasculitis, Nephritis, Arthritis;

Intravenously

53
Q

What disease occurs when Ag:Ab complexes are deposited in the perivascular area?

A

Arthus reaction

54
Q

What disease occurs when Ag:Ab complexes are deposited in the capillary/alveolar interface?

A

Farmer’s lung

55
Q

In Type III reactions, how are mast cells degranulated?

A

Ab:Ag complexes stimulate C5a to bind to mast cells or bind directly to Mast cells by FcyRIII on mast cell

56
Q

If a tetanus booster is given within 5 years of the previous booster, which hypersensitivity results? Why?

A

Type III- because already have high levels of these antibodies

57
Q

What type of hypersensitivity is associated with serum sickness? How long does it take for the symptoms to arise?

A

Type III; take approximately a week because need to get antibodies

58
Q

What are the symptoms of serum sickness?

A

Fever, vasculitis, arthritis, nephritis

59
Q

What immune component mediates Type IV hypersensitivity?

A

T cells

60
Q

What are the three different “syndromes” that result from Type IV hypersensitivities?

A

Delayed, contact, gluten sensitive enteropathy

61
Q

Type IV require more or less antigen exposure than the other hypersensitivities?

A

More

62
Q

What T cell population is involved in a delayed type hypersensitivity? What do these cells do that lead to inflammation?

A

TH1- release cytokines that recruit macrophages, increase vascular permeability

63
Q

With contact hypersensitivity what immune cells are responsible? What do they do?

A

TH lead to the activation of more cells, TC cells kill cells that are presenting the antigen

64
Q

What chemokine can increase the expression of MHC class II and therefore increase the Type IV reaction?

A

IFN-gamma

Immunology: hypersensitivity, autoimmunity, immunodeficiency (4 decks)

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