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Immuno Exam 3 > Lecture 22 > Flashcards

Lecture 22 Flashcards

1
Q

Allergy

A

altered immunological state induced by an antigenic substance resulting in pathological reactions on subsequent encounter with that antigen (or similar antigen), Type I hypersensitivity or hypersensitivity

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2
Q

Allergen

A

an antigen that stimulates IgE-mediated reactions (pollen, dust, animal dander)

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3
Q

Asthma

A

chronic occluding disease of small and large airways of the lungs that is immunologically mediated. Allergic or non-allergic (Gamma/delta TCR and eosinophils play a significant role)

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4
Q

Atopy

A

susceptibility of certain individuals to natural sensitization by environmental allergens (pollen, spores, foods)

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5
Q

Sensitization

A

the process of inducing a an immune response resulting in an untoward effect - for Type I hypersensitivities it is production go IgE

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6
Q

Hypersensitization

A

adapted immune response that occurs in an exaggerated or inappropriate form, causing damage and/or aberrant physiological functions

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7
Q

Anaphylaxis

A

adverse response provoked by an allergen, which results in vasodilation and smooth muscle relaxation in the periphery and constriction of smooth and opposite effect on smooth muscle of the bronchus and GI tract

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8
Q

Body regions with IgE localization

A

skin, respiratory and GI tract

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9
Q

Mast cell localization

A

fixed tissue near blood vessels in skin, CT, linking of gut and lungs

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10
Q

Influencers of Atopy

A

propensity of allergen, route of exposure, genetics, age

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11
Q

Type 1 Immediate Hypersensitivity - anaphylaxis Immune Pathologic Mechanism

A

IgE

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12
Q

Type 1 Immediate Hypersensitivity - anaphylaxis includes activation of which cells?

A

Mast cells, basophils, eosinophils

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13
Q

Type 1 Immediate Hypersensitivity - anaphylaxis includes which mediators

A

histamine, other vasoactive amines, arachidonic acid metabolites, cytokines

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14
Q

Type 1 Immediate Hypersensitivity - anaphylaxis includes release of

A

Oxygen and nitrogen radicals, proteases, etc

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15
Q

Examples of Type 1 Immediate Hypersensitivity - anaphylaxis include

A

Hay fever, asthma

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16
Q

Type 1: Immediate Hypersensitivity - anaphylaxis occurs within _____________ of exposure

A

15 min

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17
Q

Type II: Antibody-mediated cytotoxic or cytolytic reaction Pathological Mechanism

A

IgM, IgG antibodies against tissue or cell surface antigens

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18
Q

Type II: Antibody-mediated cytotoxic or cytolytic reaction includes activation of which cells?

A

leukocytes (neutrophils and macrophages)

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19
Q

Type II: Antibody-mediated cytotoxic or cytolytic reaction includes an abnormality in…

A

receptor function

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20
Q

Type II: Antibody-mediated cytotoxic or cytolytic reaction includes activation of?

A

complement, leukocytes (macrophages and neutrophils)

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21
Q

Examples of Type II: Antibody-mediated cytotoxic or cytolytic reaction include

A

transfusion reactions, hemolytic disease of the newborn

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22
Q

Type III: Immune Complex-Mediated Pathological Mechanism

A

Immune complexes of circulating antigens and IgM or IgG antibodies

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23
Q

Type III: Immune Complex-Mediated includes activation of?

A

complement, leukocytes

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24
Q

Type III: Immune Complex-Mediated includes release of

A

oxygen, nitrogen radicals, proteases, and cytokines

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25
Q

Examples of Type III: Immune Complex-Mediated include

A

Arthus reactions, serum sickness, certain autoimmune diseases

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26
Q

Type IV: T-cell mediated Pathological Mechanism

A

CD4+ T cells (delayed hypersensitivity), CD8+ CTLs (T cell mediated cytolysis)

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27
Q

Type IV: T-cell mediated includes activation of

A

macrophages

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28
Q

Type IV: T-cell mediated causes release of

A

cytokines, oxygen and nitrogen radicals, and proteases

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29
Q

Type IV: T-cell mediated causes

A

direct target cell lysis and scarring fibrotic response

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30
Q

Principle of IgE

A

protective role in host defense and immunity to PARASITIC infections

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31
Q

Adverse role of IgE

A

allergies, asthma, and anaphylaxis

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32
Q

Atopic serum

A

serum from a sensitized atopic patient that contains antibodies to an allergen

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33
Q

Steps of Type 1 (immediate) Hypersensitivity Response

A

Primary exposure, induction if IgE, IgE binding to receptor on mast cells and basophil, Secondary exposure, binding of allergen to cell-associated IgE and cross linking of 2 IgE Fc, signal transduction, Mediator effects

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34
Q

Primary response: Sensitization Predisposing Factors

A

propensity of allergen to induce IgE (nature of allergen, food, environment), Route of exposure (respiratory, GI, skin), genetics (HLA alleles, IL-13, IL-14, CD14, cytokine), age (very young and old)

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35
Q

Type 1 (immediate) Hypersensitivity activates IgE production by

A

activating B cells with T cell help

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36
Q

Antibody production is

A

Th2 dependent - IL-4 and IL-5 enhance B cell cell IgE response

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37
Q

IN the absence of IL-4 what other cytokine can activate the receptor to initiate an allergic response

A

IL-13

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38
Q

_______ is involved in negative control of IgE production and immediate hypersensitivity response.

A

IFN-gamma

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39
Q

What route of exposure is most likely to trigger IgE production? Why?

A

Repiratory, GI, Skin because mast cells and IgE-bearing B cells end to line the skin, mucous membranes, and connective tissue

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40
Q

What immune response and cytokine production is required for antibody production?

A

Th2 and IL-4

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41
Q

What antibody may play a protective role in preventing allergens from contacting mast cells and IgE-bearing B cells?

A

IgA

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42
Q

What polymorphisms have been linked to hypersensitivities?

A

HLA alleles, IL-13 and IL-4 receptor and CD14

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43
Q

Why are very young and some elderly patients more susceptible to hypersensitivities?

A

decreased thymus activity

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44
Q

Induction of IgE producing-B cells is Th___ dependent

A

Th2

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45
Q

What cytokine/s are involved in enhancing IgE response?

A

IL-4 and IL-5

46
Q

Which cytokine can mediate an allergic response in the absence of IL-4?

A

IL-13 (shares a receptor with IL-4)

47
Q

Which vaccine may down regulate hypersensitivity responses in humans? How?

A

BCG vaccine; shifts the immune response profile to a Th1 response

48
Q

Some believe that allergies and asthma are a deficiency in ____?

A

IFN-gamma

49
Q

Explain what atopy means.

A

a person who develops clinical symptoms after repeated exposure (10% of the population)

50
Q

High serum levels of IgE suggest

A

increased chance of hypersensitivity

51
Q

Allergic asthma is mediated by

A

gamma/delta-TCR recognition of antigens processed by CD1 molecules

52
Q

IgE binds with high affinity to

A

Fc receptors on mast cells or basophils

53
Q

Which Ig-Fc receptor interaction has the highest binding affinity?

A

IgE-Fc on mast cells and basophils, the Fc(epsilon)RI

54
Q

Fc(epsilon)RI is found on

A

mast cells and basophils

55
Q

Fc(epsilon)RII is found on? and binds ___ with ________ affinity?

A

platelets, lymphocytes, monocytes, and eosinophils; IgE with low affinity

56
Q

What cells is the main effector of Type I hypersensitivity responses?

A

mast cells

57
Q

Mast cells are located in the tissue near

A

blood vessels in skin, CT, and lining of the gut and lungs

58
Q

Mast cell morphology

A

mononuclear, granulated, basic cells in tissue

59
Q

Basophil morphology

A

polynuclear, granulated, basic cells in circulation

60
Q

What happens to the half life of IgE when bound to Fc(epsilon)RI?

A

it goes from being very short (2 d) to greatly extended

61
Q

Activation - subsequent exposure - reaction happens faster because

A

memory T and B cells exist

62
Q

Activation - subsequent exposure - Mechanism

A

allergen binds at least 2 IgE molecules on mast cells, cross-linking the IgE and causing aggregation of the Fc receptors

63
Q

Receptor aggregation causes

A

activation signal to cell

64
Q

Signal transduction involves

A

changes in membrane fluidity, actin filament formation, release of pre-formed granules, methylation of membrane phospholipids and influx of Ca, increased cAMP and cGMP

65
Q

Activation causes changes in membrane fluidity resulting in

A

destabilization of membrane

66
Q

Activation causes increased cGMP and cAMP intracellularly resulting in

A

activation of the cell to form other components de novo and slows degranulation

67
Q

Pre-formed mediators released by the Mast cells include

A

histamine, eosinophil and neutrophil chemotactic factor of anaphylaxis, neutral proteases, hydrolyses, heparin

68
Q

the role of mast cell released histamine:

A

Smooth muscle constriction of the bronchus and GI, and smooth muscle relaxation in the vasculature, increased vascular permeability and edema, pruritus, increased exocrine secretions

69
Q

the role of mast cell released eosinophil chemotactic factor and neutrophil chemotactic factor of anaphylaxis:

A

recruitment and chemotaxis of eosinophils and neutrophils (late phase cellular reactants)

70
Q

the role of mast cell released neutral proteases and hydrolases include:

A

extracellular matrix alteration via degradation (unknown reason)

71
Q

the role of mast cell released heparin

A

inhibit coagulation

72
Q

Newly synthesized mediators of activated mast cells include:

A

arachidonic acid and its by-products, Leukotrienes C, D, and B, prostaglandins, and thromboxanes, Platelet activating factor, cytokines IL-4, IL-13, TNF-alpha, IL-3 and IL-5

73
Q

Arachidonic acid is released from __________ by __________

A

cell membrane lipids by phospholipases

74
Q

the oxidation of arachidonic acid by _____________ results in the formation of _________________

A

Lipoxygenases, leukotrienes C and D and leukotriene B

75
Q

Slow-reacting substances of anaphylaxis (SRS-A) include

A

leukotrienes C and D and leukotriene B

76
Q

the role of leukotrienes C and D

A

cause smooth muscle contraction, increased vascular permeability, and mucus secretion

77
Q

the role of leukotriene B

A

chemotactic factor for neutrophils

78
Q

the oxidation of arachidonic acid by _____________ results in the formation of _________________

A

cyclooxygenases, prostaglandins and thromboxanes

79
Q

the role of prostaglandins and thromboxanes

A

vascular and smooth muscle tone, platelet aggregation and immune reactivity

80
Q

newly synthesized mediators of mast cells include platelet activating factor, which results in

A

platelet aggregation and secretion, neutrophil aggregation and degranulation, chemotaxis and release of oxygen radicals

81
Q

newly synthesized mediators of mast cells include which cytokines?

A

IL-4, IL-13, TNF-alpha, IL-3, IL-5

82
Q

The role of IL-4 and IL-13

A

further stimulation of Th2 cells and induces B cells to make IgE

83
Q

The role TNF-alpha

A

activates endothelium for the extravasation of leukocytes and promotes inflammatory response

84
Q

The role of IL-3 and IL-5

A

stimulate eosinophil growth and differentiation

85
Q

Manifestations of a mild Type I Hypersensitivity

A

Cutaneous - “wheal and flare” and urticarial rash, Respiratory - nasal congestion, pruritus, rhinitis, conjunctivitis, sneezing and coughing
Ingested - vomiting, diarrhea

86
Q

Describe the wheal and flare reaction

A

wheal: edema as a result of an increase in blood vessel permeability (formed elevation)
flare: blood vessel dilation (redness)

87
Q

Manifestations of a severe Type I Hypersensitivity

A

laryngeal edema, hypotension and shock, bronchospasm, cardiac arrhythmia, cardiorespiratory arrest

88
Q

Manifestations of asthmatic Type I Hypersensitivity

A

chronic obstructive disease of the lower airway (intrinsic or allergic)

89
Q

Asthma is mediated by 3 events:

A

reversible obstruction (mucus), bronchial hyperresponsiveness to stimuli, inflammation

90
Q

The initial Type I Hypersensitivity response occurs in

A

minutes

91
Q

The late phase Type I Hypersensitivity response occurs in

A

hours

92
Q

Type I Hypersensitivity response may be lethal by means of

A

asphyxiation from laryngeal edema, suffocation from bronchiolar constriction, shock, loss of adequate BP from overwhelming peripheral edema

93
Q

Managing an atopic reaction involves 3 steps

A

identification of an allergen, avoidance of allergen, pharmacological intervention

94
Q

How would one identify an allergen?

A

Challenge Test (Skin test): degree of wheal and flare is graded 1-4 correlating to degree of sensitivity or In vitro tests RIST and RAST

95
Q

RIST

A

measures total IgE - radioimmuo sorbent test

96
Q

RAST

A

Specific IgE - radioallergosorbent test

97
Q

If patient is atopic but yields low titers of IgE (total or specific) this may be due to

A

IgE sequestration by high affinity mast cell receptors, leaving no free IgE for detection

98
Q

If a patient is not atopic but yield high titers of IgE this may be due to

A

IgE not being sequestered on mast cells or during parasitic infections

99
Q

How would one account for IgE bound to mast cells and unbound IgE?

A

semi-quantitative assessment comparing lowest possible reaction and highest possible reaction

100
Q

Antihistamine effects

A

compete with histamine for receptor sites, preventing immediate symptoms (must be used as a PREVENTATIVE)

101
Q

Cromolyn Sodium effects

A

stabilizes the mast cell membrane preventing degranulation when administered PRIOR to exposure

102
Q

Corticosteroid effects

A

preventing the arachidonic acid pathway, preventing LATE phase reactants

103
Q

Epinephrine effects

A

treats life-threatening symptoms by reversing the effects of histamine on smooth muscle in the GI and respiratory tracts and relaxation of vasculature (β2-adrenergic receptor agonist )

104
Q

Xolair (Omalizumab)

A

humanized anti-IgE antibody, prevents the binding of IgE on mast cells Fc(epsilon)RI

105
Q

Singulair

A

leukotriene receptor antagonist, blocks the effects of leukotriene D4 on the CysLT1 receptor

106
Q

Hyposensitization Therapy

A

injection of diluted allergen, while slowly increasing concentration over time (weeks to months)

107
Q

Hyposensitization Therapy Theory

A

IgG is produced which binds the allergen preventing it form binding to IgE-bearing Mast cell

108
Q

Desensitization Therapy

A

administering very minute amounts of the allergen and increasing to larger effective doses over hours

109
Q

Desensitization Therapy Theory

A

smaller doses slowly trigger sublethal doses of histamine from mast cells, depleting them of their granules so a larger dose can be administered without lethal effects

110
Q

When would one use desensitization therapy?

A

horse serum anti venom for snakebite, antibiotic to which they are sensitized to is needed

Immuno Exam 3 (6 decks)

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