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Block 6 Week 2 Colt > Type I Hypersensitivity - Hunter > Flashcards

Type I Hypersensitivity - Hunter Flashcards

1
Q

what Ig mediates type 1 hypersensitivity?

A

IgE

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2
Q

What type of antigen is used in type 1 hypersensitivity?

A

soluble antigen

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3
Q

What is the effector mechanism of type 1 hypersensitivity?

A

Mast-cell activation and degranulation and eosinophils

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4
Q

When we think of normal hay fever allergies, what type of hypersensitivity is this

A

type 1

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5
Q

is the antigen in type 1 necessarily pathogenic?

A

no, type 1 is a response to an otherwise innocuous Ag

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6
Q

how long does a type 1 reaction take?

A

can begin within seconds, but most take minutes to hours

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7
Q

what is the evolutionary basis for a type 1 reaction?

A

protection against metazoan parasites

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8
Q

T/F: there was evolutionary pressure to create allergies

A

FUCKING FALSE

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9
Q

What cell mediates killing of worms?

A

IgE activated eosinophils

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10
Q

Cross-linking of anti-parasite IgE on (blank) cells cuases release of mediators that promote their expulsion

A

mast cells

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11
Q

by what route do allergens access the body?

A

mucosal surfaces

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12
Q

What was the selective pressure to develop IgE mediated responses?

A

Worms. Billions of people infected with worms

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13
Q 
Plant pollens
Animal dander
Mold spores
dust mite feces
these are all extrnisic allergens that are (blanked)
A

inhaled

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14
Q 
Insect venoms
vaccines
drugs
therapeutic proteins
these are all extrinsic allergens that are (blanked)
A

injected

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15
Q

food

orally administered drugs both gain access how

A

ingestion

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16
Q

Do all people respond the same way to the same allergen?

A

Nope

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17
Q

What cells in the mucosa begin the allergy response?

A

dendritic cells

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18
Q

what cytokines do DCs release when they contact allergens?

A

IL4
IL5
IL9
IL13

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19
Q

Cytokines released by DCs in response to allergies promotes what T cell differentiation?

A

TH2

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20
Q

Can you have allergies without a TH2 response?

A

NOPE

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21
Q

What class of allergen is a protein with CHO side chains, is effective at low dose, has a low Mwt., is highly soluble, stable, and binds MHCII?

A

airborne allergens

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22
Q

What is the “benefit” of airborne allergens being low dose?

A

favors activatoin of IL4 producing T cells (TH2)

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23
Q

What is the benefit of allergens with low Mwt?

A

they can diffuse into the mucosa easier

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24
Q

what is the benefit of allergens being highly soluble?

A

can readily elute from its parent particle

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25
Q

t/f: allergens can still be immunogenic even after they have been dessicated

A

true

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26
Q

why is it necessary that allergens bind MHCII?

A

Need a T cell response to elicit allergies

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27
Q

what macromolecule are allergens?

A

proteins!!

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28
Q

Describe the genetic component to allergies

A

You have to have the MHCII molecules that will be able to bind to allergens.

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29
Q

What Ig is used in type 2?

A

IgG

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30
Q

What is the Ag type in type2?

A

cells surface or matrix associated Ag

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31
Q

What is the effector mechanism for type 2?

A

Complement, FcR+ cells (phagocytes and NK cells)

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32
Q

What are two notable examples of type 2 hypersens?

A

penicillin allergies and chronic urticaria (FceRI chain)

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33
Q

When using the cell surface receptor type Ag, what is the effector mechanism for type 2?

A

Ab alters signaling

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34
Q

what Ig is used in type 3?

A

soluble Ag

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35
Q

What is the effector mechanisms of type 3?

A

complement and phagocytes

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36
Q

What is formed in type 3 that cuases vascular damage

A

immune complexes

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37
Q

What are two common reactions that are seen from type 3?

A

serum sickness and Arthus reaction

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38
Q

What hypersens type is used in most autoimmune reactions?

A

type 2

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39
Q

what sets type 4 apart from the other types?

A

its the only one that doesnt use Abs!

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40
Q

What are the three immune reactants in type 4?

A
  1. TH1
  2. TH2
  3. CTLs
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41
Q

what ag is used in type 4 Th1/

A

soluble ag

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42
Q

what is the effector mechanism in Th1 type 4?

A

macrophage activation

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43
Q

What is the ag in type 4 Th2?

A

soluble Ag

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44
Q

What is the effector mechanism for type 4 Th2?

A

IgE production, eosinophil activation, mastocytosis

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45
Q

What is the ag for CTL type 4?

A

cell-associated ag

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46
Q

what is the effector mechanism for CTL type 4?

A

cytotoxicity

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47
Q

Allergic responses involve Ig(blank) class switching of B cells

A

IgE

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48
Q

What are the two signaling systems used between T and B cells to switch to IgE?

A

IL4/IL4R

CD40/CD40L

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49
Q

Which cell carries CD40 and which CD40L?

A

CD40L: T cell
CD40: B cell

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50
Q

Which cell produces IL4 and which has the receptor?

A

T cell produces, b cell has receptor

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51
Q

From what Ig subclass are you switching to produce IgE?

A

IgM to igE

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52
Q

Can IgM cause allergies?

A

NO

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53
Q

T/F: production of IgG instead of IgE can be allergy-protective

A

true

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54
Q

is IgE free in plasma or cell-bound?

A

cell-bound, unlike other Abs

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55
Q

Does IgE have low or high plasma levels?

A

low

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56
Q

What does an elevated plasma IgE indicate?

A

the patient has allergies

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57
Q

IgE binds the FceRI receptor on which three cell types?

A
  1. mast cells
  2. basophils
  3. eosinophils
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58
Q

What protein modification does IgE have?

A

Glycosylation

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59
Q

Allergic reactions ocurr after the (first/second) exposure to Ag

A

SECOND

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60
Q

What is difference in time between DTH and type 1?

A

type 1 happens in seconds to minutes while DTH takes at least 18 hours

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61
Q

Where do you find mast cells?

A

skin, all mucosal areas, and lining the blood vessels

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62
Q

Is binding a single Ig receptor sufficient to trigger a mast cell?

A

NO, you have a threshold of stimulation where you need either multiple epitopes of one Ag or multiple Ags binding to begin signaling

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63
Q

What are the preformed mediators in mast cell granules?

A

vasoactive amines (histamine) and proteases (chymase, tryptase)

64
Q

Enzymatic modification of what lipid leads to lipid mediators?

A

arachidonic acid

65
Q

Transcriptional activation within the mast cell leads to (blank) production

66
Q

How are the granules released from the mast cell?

A

Granule exocytosis

67
Q

What are the products of the lipid mediators?

A

Prostaglandins (PGD2)

Leukotrienes (LTC4)

68
Q

How are the lipid mediators released from the mast cell?

69
Q

What cytokines do mast cells produce? How are they released?

A

TNF-a, secretion

70
Q

What is the function of the vasoactive amines?

A

vascular dilation, smooth muscle contraction

71
Q

what is the function of the proteases?

A

tissue damage

72
Q

what is the function of the prostaglandins?

A

vascular dilation

73
Q

what is the function of the leukotrienes?

A

smooth muscle contraction

74
Q

what is the function of TNF-a?

A

inflammation and leukocyte recruitment

75
Q

how long does it take for granule mediators to work?

A

seconds to minutes

76
Q

how long does it take for lipid mediators to work?

A

minutes to hours

77
Q

how long does it take for cytokines to work?

78
Q

What is the effect of mast cell activation on the GI tract? What is the clincial result?

A

increased fluid secretion, increased peristalsis.

Expulsion of GI contents (worms)

79
Q

What is the effect of mast cell activation on the ENT system? What is the clincial result?

A

decreased diameter, increased mucus secretion

Congestion and blocking of airways, swelling in nasal passages

80
Q

What is the effect of mast cell activation on the blood vessles? What is the clincial result?

A

increased blood flow and permeability
edeam leading to increased lymph flow to lymph nodes, increased cells and protein in tissue, increased effector responses, HYPOTENSION AND ANAPHYLACTIC SHOCK

81
Q

the dose and ROUTE of allergen administration determines the type of (blank)-mediated allergic reaction

82
Q

Hi dose IV Ag leads to:

A

general release of histamine, SYSTEMIC ANAPHYLAXIS

83
Q

low dose SubQ Ag leads to:

A

local release of histamine, hives

84
Q

low dose inhalation of Ag leads to:

A

allergic rhinitis, asthma

85
Q

Ingestion of ag leads to:

A

contraction of intestinal smooth muscle, outflow of fluid into gut lumen, diffuse hives or ANAPHYLAXIS

86
Q

T/F: enzymes frequently trigger allergies

87
Q

dust mite fecal protein DerP1 cleaves (blank) in tight junctions to get into the mucosa

88
Q

DerP1 is taken up by (blank) cells adn presented for (blank) cell priming

A

DCs, TH2 priming

89
Q

Where do the DCs that pick up DerP1 prime the T cells?

A

in the LYMPH NODES

90
Q

Plasma from the lymph node brings back to the mucosa that saw DerP1 what three things?

A

plasma cells
(making IgE)
mast cells

91
Q

What percent of Americans are allergic to dust mites?

92
Q

what two classes of molecules do eosinophils secrete?

A

toxic proteins

inflammatory mediators

93
Q

Eosinophilia occurs in patients with:

A

allergies!

94
Q

What cytokine induces eosinophilia?

95
Q

Eoxtaxins 1 and 2 (CCL11) bind to what eosinophil receptor?

96
Q

Do eosinophils constitutively express FceRI receptor?

A

No, only activated eosinophils!

97
Q

What type of bug do eosinophils protect against?

98
Q

describe the acute response to asthma?

A
  1. inflammatory mediators cause increased smoth muscle secretion
  2. airway obstruction from secretions
  3. recruitment of cells via TNF-a
99
Q

describe the chronic response to asthma?

A
  1. TNF-a reacts with TH2, making IL5 and eotaxin

2. Mast cells and eosinophils recruited by IL5/eotaxin

100
Q

What are the effects of chronic inflammation of the lung?

A

Airway remodeling and hyperreactivity

101
Q

T/f: most allergic reactions have both an immediate and late phase response

102
Q

What characterizes the immediate allergic reaction?

A

vasodilation, congestion, and edema

103
Q

What characterizes the late phase allergic reaction?

A

inflammatory infiltrate of eosinophils, neutrophils, and T cells

104
Q

Describe the time course and severity of the immediate vs late phase reactions?

A

immediate: short lived and high level
late: longer lasting and milder symptoms

105
Q

how long does it take to develop the immediate response?

A

minutes in a PREVIOUSLY SENSITIZED person

106
Q

how long does it take to develop the late phase?

A

2-24 hours

107
Q

Review the whole pathway of type 1 activation (7)?

A
  1. Ag exposure
  2. Activation of Th2 cells and IgE switching in B Cells
  3. Production of IgE by B cells
  4. Binding of IgE to mast cells
  5. Repeat exposure to Ag
  6. Activation of mast cells and degranulations
  7. Immediate and late phase reaction.
108
Q

What is an exaggerated IgE response called?

A

atopy, found in more than 50% of western people

109
Q

T/f; one gene is involved in atopy

A

false; a variety of genes (MHCII, FceRI receptor, Th2 cytokines)

110
Q

t/f: environmental factors influence atopy

111
Q

What is the hygeine hypothesis?

A

Exposure to microbial pathogens promotes a Th1 deviation

112
Q

Where is the MHC locus located?

113
Q

What tests do you use to determine specific allergies?

A

Intradermal or epicutaneous skin test

114
Q

What receptors do anti-histamines block?

115
Q

what is the effect of histamines on blood vessels?

A

DECREASES vascular permeability

116
Q

What is the effect of histamines on unmyelinated nerves?

A

inhibits itching

117
Q

what receptor does albuterol bind?

A

B-adrenergic

118
Q

what is the effect of albuterol?

A

relaxes bronchial smooth muscle

119
Q

What is the mechanism of action of Singulair?

A

Blocks leukotrienes D4, C4, and E4; inhibits bronchoconstriction

120
Q

what are the effects of epinephrine?

A

relaxes bronchial smooth muscle, constricts vascular smooth muslce, reforms endothelial tight junctions

121
Q

Systemic and topical corticosterioids suppress (acute/chronic) inflammation

122
Q

What is the mechanism of actino of corticosteroids/

A

block NF-kb thereby blocking transcription of proinflammatory genes

123
Q

T/F: mast cells are important in immunity for things other than parasites

A

true: viruses and bacteria as well.

124
Q

What drugs would you use to control mediator actions?

A

antihistamines, B-blockers, lipoxygenase inhibitors

125
Q

What drugs would you use to control chronic inflammatory reaction

A

corticosteroids

126
Q

What drugs would you use to control a TH2 response?

A

desensitization therapy by injections of specific antigens

127
Q

What drugs would you use to control IgE binding to mast cells?

A

Anti-IgE Abs

128
Q

In desensitization, you are shifting from IgE to (blank)

129
Q

How is cross-linking of IgE prevented in desensitization?

A

anti-allergen IgG binds up the allergen

130
Q

What T cell type is produced during desensitization?

A

Tregs; secrete IL10 and TGf-b that promote isotype switching

131
Q

omalizumab humanized mouse anti-IgE blocks IgE binding to the (blank) receptor ton mast cells, basophils, and eosinophils

132
Q

What is the most common chronic skin disease in young children?

A

atopic dermatitis (eczema)

133
Q

T/F: most patients with AD are atopic

134
Q

What two bugs commonly colonize and infect pts with AD?

A

staph aureus and herpes simplex virus

135
Q

Elevated serum (blank) is seen in 80-85% of patients with AD

136
Q

(blank) cells are also elevated in AD, along with elevated TH2 cytokines (which calls these cells to the sites)

A

Eosinophils

137
Q

What is the Tx of AD?

A

avoidance of irritants and allergens, topical corticosteroids

138
Q

Where does eczema normally present?

A

around the cheeks and mouth, moves then to trunk and extremities.

139
Q

What is the “itch that rashes”?

140
Q

Anaphylaxis to insect stings occurs in what percent of people?

A

3% of adults; 1% of kids

141
Q

sensitization to insect venom is seen in what percent of adults?

142
Q

How do you diagnose insect sting allergies?

A

Venom skin tests and venom specific IgE immunoassays

143
Q

What is the efficacy of venom immunotherapy?

144
Q

These are examples of what?

  1. Anaphylaxis from b-lactam antibiotcs
  2. halthane hepatitis
  3. hypotension post protamine
  4. dermatitis from sulfonamides
  5. serum sickness form phenytoin/cefaclor
  6. hypotension after succinylcholine
  7. quinine induced thrombocytopenia
  8. phenophthalein induced fixed drug eruption
  9. Cisplatinum urticaria
A

IgE mediated drug hypersensitivity

145
Q

drugs like penicillin can directly bind with macromolecules on cell surfaces forming (blank)

A

hapten-carrier complexes

146
Q

Describe the concept of multivalency related to drug haptenation?

A

Multiple drug epitopes must bind at a threshold level to induce a drug specific immune response

147
Q

The b-lactam ring in penicillin will cause what kind of reaction of lysine in proteins?

148
Q

Is a hapten immunogenic on its own?

A

No, it must be conjugated to a protein

149
Q

When penicilloyl haptens are taken up into MHC II in the presence of a danger signal from infection, (blank) cells are activated

A

CD4 T cells

150
Q

The hapten activated CD4 T cell activates specific b cells to produce (blank)

A

IgE anti-penicilloyl Abs

151
Q

What antibiotics share the b-lactam ring?

A

1.penicillin
2.carbapenems
3.cephalosporins
4.monobactams
ALL OF THESE CAN CAUSE ALLERGIC CROSS REACTIONS

152
Q

anti-penicillin IgE arms what type of cells?

A

mast cells

153
Q

What type of exposure route is the greatest antigenic load to the immune system?

154
Q

T/F: most people develop tolerance to food allergies?

155
Q

T/F: peanut allergies have tripled in the past decade in western countries

156
Q

what is the only proven therapy for food allergies?

A

strict avoidance

157
Q

What is the most common form of food allergy?

Block 6 Week 2 Colt (3 decks)

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