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Immunology Block 2 > 16: Hypersensitivity Reactions > Flashcards

16: Hypersensitivity Reactions Flashcards

1
Q

Hypersensitivity

A

A state of heightened reactivity to antigen

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2
Q

Hypersensitivity reactions

A

Immune responses to innocuous antigens that lead to symptomatic reactions upon re-exposure

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3
Q

Hypersensitivity disease

A

Damage to host tissue caused by hypersensitivity reactions to typically innocuous antigens

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4
Q

Who classified hypersensitivity reactions into 4 types based on the types of antigens that are recognized and the types of immune responses involved?

A

Coombs and Gel

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5
Q

What does Type I hypersensitivity involve?

A

IgE-dependent triggering of mast cells

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6
Q

What does Type II hypersensitivity involve?

A

IgG antibody that is reactive with cell-surface or matrix antigens

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7
Q

What does Type III hypersensitivity involve?

A

Production of antigen:antibody complexes

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8
Q

What does Type IV hypersensitivity involve?

A

T cell-mediated hypersensitivity

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9
Q

Antigens that selectively stimulate TH2 cells that drive an IgE response are known as ______.

A

Allergens

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10
Q

What are the features that many allergens have in common? (4)

A
  1. Small proteins
  2. Highly soluble
  3. Carried on desiccated particles
  4. Upon contact with mucosa of airways, soluble antigens elute from the delivery particles and diffuse into the mucosa
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11
Q

Antigens presented to TH0 cells at low doses tend to elicit differentiation into ________.

A

TH2 CD4 cells

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12
Q

T or F: All common allergens have enzymatic activity.

A

F: most but not all

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13
Q

What is the prerequisite for type I hypersensitivity?

A

The initial response to an allergen must be an IgE response

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14
Q

What cytokines do TH2 cells produce that favor class switching to IgE?

A

IL-4, IL-5, and IL-13

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15
Q

What do TH2 cells do to favor class switching to IgE?

A
  1. Produce and secrete IL-4, IL-5, and IL-13

2. Upregulate expression of CD40L and CD23

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16
Q

What kind of cells primarily initiate type I hypersensitivity reactions?

A

Mast cells

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17
Q

What types of cells have FCeRI receptors?

A

Mast cells, eosinophils, and basophils

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18
Q

What is atopy?

A

A predisposition to allergy

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19
Q

T or F: Atopic individuals have higher levels of soluble IgE and more circulating eosinophils than non-atopic individuals.

A

T

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20
Q

Genes encoded on chromosomes ____ and ___ appear to be involved in allergic predisposition.

A

5 and 11

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21
Q

Chromosome 11 encodes a gene for _______.

A

The beta subunit of FCeRI

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22
Q

Chromosome 5 encodes a cluster of genes that encode _____________.

A

Proteins involved in isotype switching, eosinophil survival, and mast cell proliferation (IL-3, IL-4, IL-5, IL-9, IL-13, and GM-CSF)

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23
Q

T or F: HLA Class II polymorphism affects the IgE response to certain allergens.

A

T

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24
Q

What is the wheal and flare reaction?

A

An inflammatory reaction produced immediately at the injection site that is a result of mast cell degranulation in the skin

  • Swelling due to increased permeability produces the wheal
  • Redness is the flare
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25
Q

The late phase reaction to an allergen is mediated by _________.

A

Leukotrienes, chemokines, and cytokines produced by mast cells following IgE-mediated activation

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26
Q

What differentiates the late phase reaction from the wheal and flare reaction?

A

Late phase reaction is 6-8 hours post injection and consists of more widespread swelling

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27
Q

Airborne allergens irritate _______ and food-borne allergens irritate _______.

A

Airborne: Irritate mucosa of respiratory tract

Food-borne: Irritate mucosa of GI tract

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28
Q

What mechanisms have developed as a means of expulsion of parasites from the body?

A

Coughing and sneezing, vomiting, diarrhea

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29
Q

What is systemic anaphylaxis?

A

Wide-spread activation of mast cell degranulation causing both an increase in vascular permeability and a widespread constriction of smooth muscle

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30
Q

What is the most common cause of anaphylaxis?

A

IgE-mediated allergy to penicillin or other drugs

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31
Q

What is the treatment for anaphylactic and anaphylactoid reactions?

A

Injection of epinephrine

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32
Q

How doe epinephrine treat anaphylactic and anaphylactoid reactions?

A

It stimulates reformation of tight junctions between endothelial cells, reducing permeability of blood vessels, diminishing tissue swelling, raising blood pressure, and stimulating the heart

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33
Q

What is allergic rhinitis?

A

Mild allergic response characterized by sneezing and runny nose in response to inhaled allergens; caused by allergens that diffuse across the mucous membranes of nasal passages and activate mucosal mast cells beneath the nasal epithelium

34
Q

What is allergic asthma?

A

A serious condition where allergic reactions to commonly inhaled allergens cause chronic breathing difficulties

35
Q

When is allergic asthma triggered?

A

When submucosal mast cells in the lower respiratory tract are stimulated by allergen/IgE interaction

36
Q

What is the overall effect of an allergic asthmatic attack?

A

Trapping of air in the lungs, making breathing more difficult (can be fatal!)

37
Q

What type of hypersensitivity reaction is chronic asthma?

A

Type IV because it can be exacerbated by immune responses to bacterial or viral infection of the respiratory tract (especially infections that elicit TH2 responses)

38
Q

Urticaria

A

Hives – caused by release of histamine by mast cells in the skin

39
Q

Angioedema

A

Inflammation caused by activation of mast cells in deep subcutaneous tissue – swelling is more diffuse than observed for urticaria

40
Q

What are the 3 strategies used to reduce the effects of allergic disease?

A
  1. Modification of patient’s behavior and environment
  2. Pharmacological approach
  3. Immunological treatment
41
Q

How do antihistamines work?

A

They prevent histamine from binding to H1 histamine receptors on vascular endothelium – reduce rhinitis and urticaria

42
Q

How do corticosteroids work for hypersensitivity?

A

They suppress leukocyte function and are used to treat chronic inflammation of asthma, rhinitis, or eczema

43
Q

How does cromolyn sulfate work for hypersensitivity?

A

It’s used as a prophylactic inhalant and it prevents degranulation of activated mast cells and granulocytes

44
Q

How does desensitization work?

A

It modulates the immune response to shift it to an IgG response. Give a series of injections with increasing doses of allergen to change the TH2 response to a TH1 response

45
Q

What type of vaccine would you give to someone to reduce hypersensitivity?

A

Vaccination with allergen-derived peptides that are known to be presented by HLA class II molecules to TH2 CD4 cells in an attempt to induce anergy

46
Q

T or F: Most IgE induced is parasite-specific.

A

F: only a small percentage is parasite-specific, the remainder is highly heterogeneous and represents the product of a non-specific polyclonal B and T cell activation by the parasite

47
Q

Who wins in competition for binding to FCeRI receptors: nonspecific IgE or parasite-specific IgE?

A

Nonspecific IgE

48
Q

Type II hypersensitivity reactions can be associated with the administration of what drugs?

A

Penicillin, quinidine, and methyldopa

49
Q

How do drugs cause type II hypersensitivity?

A

The chemically active drugs bind to the surface of RBCs or platelets and create new epitopes to which the immune system is not tolerant

50
Q

In penicillin-induced hypersensitivity, new epitopes generated by penicillin stimulate the production of ____ and ____ antibody specific for the new epitopes.

A

IgG and IgM

51
Q

What is the end result of penicillin-induced type II hypersensitivity?

A

Destruction of RBCs

52
Q

Type III hypersensitivity reactions are caused by __________.

A

Immune complexes formed from IgG and soluble antigens

53
Q

What is more efficient at fixing complement: large immune complexes or small immune complexes?

A

Large immune complexes

54
Q

Small immune complexes tend to ___________.

A

Remain in circulation and become deposited along blood vessel walls

55
Q

What is an Arthus reaction?

A

An inflammatory response created by a type III hypersensitivity reaction

56
Q

How can systemic type III hypersensitivity reactions be caused?

A

By IV administration of large quantities of antigen

57
Q

How do you get serum sickness?

A

From immune responses to non-self material administered into the bloodstream as a treatment for a variety of illnesses. It is caused by a systemic accumulation of immune complexes.

58
Q

What are the 6 characteristics of serum sickness?

A
  1. Chills
  2. Fever
  3. Rash
  4. Arthritis
  5. Vasculitis
  6. Glomerulonephritis (sometimes)
59
Q

What do transplant patients often receive to prevent rejection of transplanted tissues?

A

Large doses of monoclonal anti-T cell antibodies

60
Q

Heart attack patients receive large injections of _______ to help degrade blood clots.

A

Streptokinase

61
Q

Type III hypersensitivity can result from continual inhalation of antigens that ________.

A

Elicit IgG instead of IgE antibody responses

62
Q

What are examples of type III hypersensitivities that result from workers being exposed to the same airborne antigens daily.

A

Farmer’s lung and bird-breeders disease

63
Q

Type IV hypersensitivity reactions are mediated by _______.

A

Antigen-specific effector T cells

64
Q

Type IV hypersensitivity reactions are also known as _____________.

A

Delayed-type hypersensitivity (DTH) – different than Ab-mediated hypersensitivities which are apparent within a couple minutes of antigen exposure

65
Q

T or F: DTH reactions require much larger quantities of antigen due to inefficiency of antigen processing/presentation.

A

T

66
Q

What are the most common antigens that elicit DTH responses?

A

Mycobacterial proteins, insect venoms, penadecacatechol (poison ivy), and small metal ions

67
Q

What is the most well studied example of a type IV hypersensitivity reaction?

A

Tuberculin reaction (to test is someone has been infected with mycobacteria tuberculosis)

68
Q

What is the response to initial contact with poison ivy?

A

Production of effector T cells and immunological memory, but little if any inflammatory response

69
Q

What does penadecacatechol do upon initial contact with a poison ivy plant?

A

It penetrates the outer layers of the skin and forms covalent bonds with EC proteins and skin cell surface proteins, forming new antigens that are recognized as non-self. APCs take up the new antigens, return to secondary lymphoid tissues, and present peptide antigens on MHC Class II to naive CD4 cells. (or CD8 cells too!)

70
Q

After initial exposure to poison ivy, each subsequent contact results in a rash that is mediated by _________.

A

Antigen-specific effector CTLs and antigen-specific TH1 cells that produce cytokines for macrophage activation and induction of inflammation

71
Q

Why is poison ivy an example of contact sensitivity?

A

Because contact of the allergen with the skin is required to initiate the allergic response

72
Q

What biological effects do tryptase, chymase, cathepsin G, and carboxypeptidase have?

A

Remodeling of connective tissue matrix

73
Q

What do IL-4 and IL-13 do?

A

Stimulate and amplify the TH2-cell response

74
Q

What do IL-3, IL-5, and GM-CSF do?

A

Promote eosinophil production and activation

75
Q

What does TNF-alpha do?

A

Pro-inflammatory cytokine

76
Q

What does CCL3 do?

A

It’s chemotactic for monocytes, macrophages, and neutrophils

77
Q

What do LTC3, LTD4, and LTE4 do?

A

Cause smooth muscle contraction, increase vascular permeability, and cause mucus secretion

78
Q

What does PAF do?

A

It’s chemotactic for leukocytes, amplifies production of lipid mediators, activates neutrophils, eosinophils, and duhhh platelets

79
Q

What does mast cell granule release do in the GI tract?

A

Causes increased fluid secretion and peristalsis –> vomiting, diarrhea

80
Q

What does mast cell granule release do to airways?

A

Decreases diameter and increases mucus secretion

Immunology Block 2 (7 decks)

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