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MF2 Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Type of hypersensitivity with this pathologic immune mechanism:
Th2 cells, IgE, mast cells, eosinophils

A

Immediate hypersensitivity (Type I)

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2
Q

Type of hypersensitivity with this pathologic immune mechanism:
IgM, IgG antibodies against cell surface or extracellular matrix antigens

A

Antibody-mediated diseases (Type II)

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3
Q

Type of hypersensitivity with this pathologic immune mechanism:
Immune complexes of circulating (soluble) antigens and IgM or IgG deposited in vascular basement membrane

A

Immune complex-mediated diseases (Type III)

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4
Q

Type of hypersensitivity with this pathologic immune mechanism:
Cytokine-mediated inflammation (CD4+ T cells)
T-cell mediated killing (CD8+ CTLs)

A

T cell-mediated diseases (Type IV)

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5
Q

Type of hypersensitivity with this mechanisms of tissue injury and disease:
Mast cell-derived mediators (vasoactive amines, lipid mediators, cytokines)
Cytokine-mediated inflammation (eosinophils, neutrophils)

A

Immediate hypersensitivity (type I)

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6
Q

Type of hypersensitivity with this mechanisms of tissue injury and disease:
Complement and Fc receptor-mediated recruitment and activation of leukocytes (neutrophils, macrophages)
Opsonization and phagocytosis of cells
Abnormalities in cellular function (e.g. hormone receptor signaling)

A

Antibody-mediated diseases (Type II)

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7
Q

Type of hypersensitivity with this mechanisms of tissue injury and disease:
Complement and Fc receptor-mediated recruitment and activation of leukocytes

A

Immune complex-mediated diseases (Type III)

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8
Q

Type of hypersensitivity with this mechanisms of tissue injury and disease:
Macrophage activation, cytokine-mediated inflammation
Direct target cell lysis, cytokine-mediated inflammation

A

T cell-mediated diseases (Type IV)

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9
Q

Allergy responses rely on these being present

A

Antibodies

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10
Q

Allergy responses rely on this occurring

A

Cross linking

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11
Q

The primary determinant of a vigorous IgE response to an allergen

A

IL-4

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12
Q

These cells produce cytokines that tell the B cells to isotype switch to IgE in type I hypersensitivity

A

Th2 cells

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13
Q

Fc receptor of IgE

A

FceRI

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14
Q

FceRI is a receptor for this

A

IgE

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15
Q

These cells degranulate when antigen-specific IgE cross-links its Fc receptor

A

Mast cells

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16
Q

Mast cells are different from basophils in that they exist in:

A

Tissues

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17
Q

Basophils are different from mast cells in that they exist in:

A

Blood

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18
Q

Two similar types of cells that have granules which contain histamine

A

Mast cells and basophils

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19
Q

Mast cells possess 50-200 of these which contain effector molecules and are ready for release upon cross-linking of Fc receptor

A

Cytoplasmic granules

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20
Q

3 types of products preformed in mast cell granules

A

Enzymes (tryptase, chymase, cethepsin G, carboxypeptidase - remodel connective tissue matrix)
Toxic mediators (histamine, heparin - poison parasites, increase vascular permeability, cause smooth muscle contraction)
Cytokine (TNF-alpha - promotes inflammation, stimulates cytokine production by many cells, activates endothelium)

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21
Q

2 toxic mediators preformed in mast cell degranulations

A

Histamine and heparin

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22
Q

Cytokine preformed in mast cell granules which promotes inflammation, stimulates cytokine production by many cell types, and activates endothelium

A

TNF-alpha

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23
Q

Two cytokines released by mast cells (but not preformed in granules) that stimulate and amplify Th2 response

A

IL-4 and IL-13

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24
Q

3 Cytokines released by mast cells (but not preformed in granules) that promote eosinophil production and activation

A

IL-3, IL-5, GM-CSF

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25
Q

Chemokine released by mast cells (but not preformed in granules) that attracts monocytes, macrophages, and neutrophils

A

CCL3

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26
Q

Lipid mediators released by mast cells (but not preformed in granules) that cause smooth muscle contraction, increase vascular permeability, and cause mucus secretion

A

Leukotrienes C4, D4, E4

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27
Q

Lipid mediator released by mast cells (but not preformed in granules) that attracts leukocytes, amplified production of lipid mediators, activates neutrophils, eosinophils, and platelets

A

Platelet-activating factor

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28
Q

The following are effects of this type of cell mediators:
Vascular dilation, smooth muscle contraction
Tissue damage
Vascular dilation
Inflammation (leukocyte recruitment)

A

Mast cell mediators

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29
Q

Word for swelling that occurs at site of inoculation with an allergy during skin testing

A

Wheal

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30
Q

Word for redness that occurs at site of inoculation with an allergy during skin testing

A

Flare

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31
Q

This response can be seen within minutes (due to mast cell degranulation) after inoculation with allergen during skin testing

A

Wheal and flare reaction

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32
Q

Subcutaneous allergic reactions are characterized by the raised swelling (wheal) and redness (flare) that occur at the site within 20 minutes of intradermal exposure, and effects are mediated by this

A

Histamine
(mast cell degranulation)

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33
Q

Immediate or late phase reactions are IgE mediated and part of type I response?

A

Both

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34
Q

Late-phase reaction during skin allergen testing occur due to these 3 things synthesized by mast cells after the immediate phase of the response

A

Leukotrienes
Chemokines
Cytokines

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35
Q

This part of the wheal-and-flare reaction is caused by edema resulting from the histamine-induced capillary permeability

A

Wheal

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36
Q

This part of the wheal-and-flare reaction is caused by vasodilation and increased blood flow

A

Flare

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37
Q

Does vasodilation or vasoconstriction occur during type I hypersensitivity?

A

Vasodilation
Causes flare (redness)

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38
Q

Treatment of type I hypersensitivities focus on blocking the effects of these

A

Inflammatory mediators
(e.g. drugs that inhibit histamine and leukotrienes)

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39
Q

Food allergens are associated with localized _____ release that leads to diffusion of Ag into blood vessels
This can lead to smooth muscle contraction that induces vomiting and diarrhea
When a food or drug allergen gets carried to the skin within the bloodstream, urticaria and angioedema can develop (in some cases as precursors to systemic anaphylaxis)

A

Histamine

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40
Q

Allergic reactions in the lung involve recruitment of these cells which are not typically present in healthy tissue

A

Eosinophils

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41
Q

This stimulates the reformation of tight junctions between endothelial cells, reducing permeability and preventing fluid loss from blood, which diminishes tissue swelling and raises blood pressure
Also relaxes constricted bronchial smooth muscle and stimulates the heart

A

Epinephrine

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42
Q

This is almost always the treatment for anaphylactic shock

A

Epinephrine

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43
Q

Fall in blood pressure (shock) caused by vascular dilation; airway obstruction due to laryngeal edema and bronchial construction
Almost always treated with epinephrine

A

Anaphylaxis

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44
Q

Activated mast cells secrete this, which induces eosinophil production from bone marrow

A

IL-5

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45
Q

Activated mast cells secrete IL-5, which induces bone marrow to produce these cells

A

Eosinophils

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46
Q

These 4 chemokines interact with CCR3 receptor expressed by eosinophils to attract them to site of allergen exposure

A

CCL5, CCL7, CCL11, and CCL13

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47
Q

chemokines CCL5, CCL7, CCL11, and CCL13 interact with this on eosinophils to attract them to site of allergen exposure

A

CCR3 receptor

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48
Q

What is the role of CCR3 receptor?

A

Is on eosinophils and interacts with CCL5, CCL7, CCL11, and CCL13 to attract them to site of allergen exposure

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49
Q

The most important chemokine for eosinophils, is produced by activated endothelial cells, T cells, and monocytes

A

CCL11 (eotaxin)

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50
Q

3 types of cells that produce CCL11 (eotaxin)

A

Activated endothelial cells, T cells, and monocytes

51
Q

What is the role of CCL11?

A

is an eotoxin
the most important chemokine for eosinophils

52
Q

Unlike mast cells, resting eosinophils do not express this on their surface, and thus do not naturally coat themselves with IgE

53
Q

The presence of these cells is typically associated with chronic allergic inflammation (e.g. chronic asthma)

A

Eosinophils

54
Q

Enzymes and toxic proteins released by ______ have the potential to induce more damage than those released from mast cells

A

Eosinophils

55
Q

Enzymes and toxic proteins released by eosinophils have the potential to induce more damage than those released from ______

A

Mast cells

56
Q

3 cytokines that amplify eosinophil by bone marrow and cause eosinophil activation

A

IL-3, IL-5, GM-CSF

57
Q

Lipid mediators that cause smooth muscle contraction, increase vascular permeability, and cause mucus secretion
Are produced by eosinophils but not preformed in granules

A

Leukotrienes C4, D4, E4

58
Q

In chronic responses, these two types of cells help activate the eosinophils to cause tissue damage, recruitment of inflammatory cells (i.e. neutrophils), and irreversible damage to the airways, all of which are characteristic of chronic asthma

A

Mast cells and Th2 cells

59
Q

Chronic asthma can develop into this type of hypersensitivity

60
Q

What is the difference between chronic asthma and allergic asthma?

A

Chronic asthma involves a hyper-responsiveness and hyper-reactivity of the airways, and exposure to the allergen is no longer needed to initiate an asthma attack

61
Q

Chronic asthma primarily involves this type of cell

A

Th2 cells
IgE is no longer the immune reactant

62
Q

Therapy for anaphylaxis that causes vascular smooth muscle contraction, increases cardiac output (to counter shock), and inhibits bronchial smooth muscle cell contraction

A

Epinephrine

63
Q

Treatment for asthma that reduces inflammation

A

Corticosteroids

64
Q

Treatment for asthma that relaxes bronchial smooth muscle and reduces inflammation

A

Leukotriene antagonists

65
Q

Repeated administration of low doses of allergens as treatment for allergic diseases

A

Desensitization

66
Q

Treatment for allergic diseases that block actions of histamine on vessels and smooth muscles

A

Antihistamines

67
Q

Treatment for allergic diseases that inhibits mast cell degranulation by stabilizing their membrane (blocks the release of histamine)

68
Q

Difference between antihistamines and cromolyn

A

Antihistamines block actions of histamine on vessels and smooth muscles
Cromolyn inhibits mast cell degranulation and thus blocks the release of histamine

69
Q

Corticosteroid therapy reduces these 5 molecules

A

Cytokines
NOS
Prostaglandins
Leukotrienes
Adhesion molecules

70
Q

While corticosteroid therapy reduces cytokines (reducing inflammation), NO, decreases prostaglandin and leukotrienes, and adhesion molecules, it results in the induction of these as well, leading to induction of apoptosis in lymphocytes and eosinophils

A

Endonucleases

71
Q

Desensitization involves repeated administration of low doses of Ag in an attempt to drive immunity in this direction

A

Away from IgE and toward IgG

72
Q

Penicillin binding to this leads to an opening of the beta-lactam ring, which forms a covalent bond with a residue in the active site, thus inactivating the enzyme

A

Bacterial transpeptidase

73
Q

Penicillin is an example of a hapten-carrier system, meaning?

A

Penicillin becomes immunogenic when it binds to carrier proteins
Penicillin combines with the erythrocyte surface, acting as a hapten. This induces an antibody response directed against the penicillin-coated erythrocyte membrane.

74
Q

Penicillin binding to bacterial transpeptidase leads to an opening of this, which forms a covalent bond with a residue in the active site of the transpeptidase, thus inactivating the enzyme

A

Beta-lactam ring

75
Q

Penicillin-reactive antibodies can be either of these

A

IgE or IgG
This can lead to type I, II, or III hypersensitivity

76
Q

Type II hypersensitivities are mediated by _____ that is directed toward cell surface antigens

77
Q

In type II hypersensitivity to penicillin, complement-coated penicillin-modified ______ are phagocytosed by macrophages using their complement receptor

A

Erythrocytes cells
Macrophages then present peptides to CD4 T cells, which become Th2 cells that activate B cells to become plasma cells secreting IgG

78
Q

ABO blood group antigens are this type of hypersensitivity

79
Q

ABO blood group antigens are ______ that coat erythrocytes

A

Glycolipids

80
Q

ABO blood group antigens are glycolipids that coat these

A

Erythrocytes

81
Q

Hemolytic disease of the newborn is an example of this type of hypersensitivity

82
Q

Type III hypersensitivity involves IgG toward ____ antigens

83
Q

During a type III hypersensitivity, binding of immune complex to this on mast cell induces degranulation

84
Q

Arthus reaction involves local inflammation, increased fluid and protein release, and blood vessel occlusion, and is an example of this type of hypersensitivity

85
Q

In Arthus reaction (type III hypersensitivity), accumulation of these leads to complement fixation

A

Immune complexes

86
Q

In Arthus reaction (type III hypersensitivity), accumulation of immune complexes leads to this

A

Complement fixation

87
Q

The Arthus reaction (type III hypersensitivity) is associated with these antibodies

A

IgG (not IgE)
but it involves mast cell degranulation (FcyRIII receptors)

88
Q

This is common at the site of injection of individuals receiving inoculations for desensitization (induced IgG reacts with mast cells and injection site)

A

Arthus reaction

89
Q

Hemorrhaging in the skin and urticarial rashes can develop during these hypersensitivity reactions

90
Q

Serum sickness is this type of hypersensitivity

91
Q

Type of type III hypersensitivity involving passive transfer of antibodies from a different species used to treat infections
Immune response toward antibodies from foreign species

A

Serum sickness
Today, antivenin and IVIG represent common sources of serum sickness

92
Q

Antivenin and IVIG represent common sources of this

A

Serum sickness

93
Q

Type of Type IV hypersensitivity reaction:
Insect venom and mycobacterial proteins can be antigens
Leads to local skin swelling (erythema, induration, cellular infiltrate, dermatitis)

A

Delayed-type hypersensitivity

94
Q

Type of Type IV hypersensitivity reaction:
Pentadecacatechol (poison ivy), DNFB, and small metal ions (nickel, chromate) can be antigens
Leads to local epidermal reaction (erythema, cellular infiltrate, vesicles, intraepidermal abscesses)

A

Contact hypersensitivity

95
Q

Type of Type IV hypersensitivity reaction:
Gliadin can be antigen
Leads to villous atrophy in small bowel, malabsorption

A

Gluten-sensitivity enteropathy (celiac disease)

96
Q

Delayed-type hypersensitivity is this type of hypersensitivity

97
Q

Contact hypersensitivity is this type of hypersensitivity

98
Q

Gluten-sensitivity enteropathy (celiac disease) is this type of hypersensitivity

99
Q

Delayed type hypersensitivity takes this long to peak

A

2-3 days
Instead of minutes-to-hours like the other hypersensitivities

100
Q

Type of hypersensitivity that takes 2-3 days to peak and require 100-1000 times more Ag than others

A

Delayed type hypersensitivity (type IV)

101
Q

Delayed type hypersensitivity primarily involves this type of cell

102
Q

In a delayed type hypersensitivity, Th1 cells release this, which activates macrophages, increasing release of inflammatory mediators

103
Q

In a delayed type hypersensitivity, Th1 cells release these, which lead to local tissue destruction and increased expression of adhesion molecules on local blood vessels

A

TNF-a and LT

104
Q

In a delayed type hypersensitivity, Th1 cells release these, which leads to monocyte production by bone marrow stem cells

A

IL-3 and GM-CSF

105
Q

Delayed type hypersensitivity can involve these 2 antigens

A

Insect venom
Mycobacterial proteins (tuberculin, lepromin)

106
Q

Contact hypersensitivity can involves these 3 antigens

A

Pentadecacatechol (poison ivy)
DNFB
Small metal ions (nickel, chromate)

107
Q

Contact hypersensitivity to poison ivy can be induced by physical contact with this

A

The hapten pentadecacatechol

108
Q

In Contact hypersensitivity, the hapten pentadecacatechol forms a covalent bond with these

A

Extracellular matrix proteins

109
Q

Dendritic cells in the skin

A

Langerhans cells

110
Q

Contact hypersensitivity can occur with bivalent nickel ions that chelated by this in human proteins

111
Q

Contact hypersensitivity due to poison ivy can lead to the activation of these 2 types of cells

A

Th1 cells (via MHC II)
CD8 T cells (when pentadecacatechol crosses the plasma membrane and chemically modified intracellular protein, leading to MHC I presentation)

112
Q

There is a strong genetic predisposition to celiac disease, and it has been tracked molecularly to transglutaminase modification of this

A

Glutamine (Q) residues to glutamate (E)

113
Q

In Celiac disease, there is peptide loaded onto either of these

A

HLA-DQ2 or HLA-DQ8

114
Q

In Celiac disease, peptide is loaded onto HLA-DQ2 or HLA-DQ8, and effector T cells of this lineage

115
Q

All celiacs make these types of antibodies toward tissue transglutaminase, and many make anti-gliadin antibodies

A

IgG or IgA

116
Q

All celiacs make IgG or IgA toward this

A

Tissue transglutaminase

117
Q

All celiacs make IgG or IgA toward tissue transglutaminase, and many also make antibodies to this as well

A

Anti-gliadin antibodies

118
Q

Type of reaction to penicillin that involves urticaria and systemic anaphylaxis

A

Type I (IgE)

119
Q

Type of reaction to penicillin that involves hemolytic anemia

A

Type II (IgM, IgG)

120
Q

Type of reaction to penicillin that involves serum sickness and glomerulonephritis

A

Type III (IgG)

121
Q

Type of reaction to penicillin that involves contact dermatitis

A

Type IV (Tdth cells)

122
Q

Type IV hypersensitivity that involves macrophage activation and is seen in contact dermatitis or tuberculin reaction, utilizes these type of T cells

123
Q

Type IV hypersensitivity that involves eosinophil activation and is seen in chronic asthma and chronic allergic rhinitis, utilizes these types of T cells

MF2 Immunology (21 decks)

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