Chapter 20 - Allergy Flashcards

1
Q

what do allergic responses result from?

what are immune responses driven by? how are they carried? what activity do they contain?

A

harmful immune responses

non-infections Ags carried in particles, have protease activity

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2
Q

what kind of groups comprise allergens?

A

proteins and glycoproteins

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3
Q

what 2 ways do allergens activate the innate immune response?

A

intrinsic enzymatic activity

activation of PRRs

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4
Q

indoor allergens are associated with?

outdoor allergens?

A

asthma

allergic rhinitis

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5
Q

what are the sources of airborne proteins or glycoproteins?

A

tree and grass pollen
mold spores
animal dander
dust mite or cockroach secretions

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6
Q

what are 2 forms of dominant source allergens?

A

timothy grass pollen (UK)

birch pollen (Sweden)

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7
Q

what influences the development of atopy?

A

genetic factors (polymorphisms)

environmental factors (sensitization, # siblings, hygiene, vacc)

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8
Q

what effects Th2-mediated allergic inflammation?

A

Defects in target organs (skin, gut, bronchi)

Triggers (viral infections, allergen exposure, smoke, pollutants)

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9
Q

what are some factors favoring Th1 protective immunity?

A

TB, older siblings, day care exposure, farm life

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10
Q

What are some factors favoring Th2 phenotype leading to allergic diseases?

A

antibiotic use, diet, sensitization to dust mites, urban (thug) life

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11
Q

what is the risk of passing on atopic trait if both parents are atopic?

1 parent?

0 parents

A

75%

50

15

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12
Q

polymorphisms in what genes are known to cause atopy?

A

Beta chain of FcERIBeta
IL-4 gene
HLA-DR alleles
CD14

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13
Q

what is CD14, what does a polymorphism in it promote?

A

part of receptor for LPS

hypersensitivity

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14
Q

patients with ragweed pollen allergy have IgE and IgG hypersensitivity due to what allelic association?

A

HLA-DR2

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15
Q

what does high levels of IgE in the cord blood of infants predict?

A

future development of atopy

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16
Q

what is the main postulate of the hygiene hypothesis?

A

the increased incidence of allergy is associated with the decrease in exposure to common infections during early life

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17
Q

how can atopic (Th2) phenotype be prevented?

A

Th1 type response

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18
Q

what can limit the development of unrelated allergen-mediated disease?

A

increased # of Tregs

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19
Q

Anaphylaxis is what type of hypersensitivity?
what Ags and what effectors does it display?
what kind of damage is it associated with?

A

Type I, Ag: insect venoms, drugs, food
Effectors: IgE on basophils and mast cells
oedema, bronchoconstriction, vascular collapse, death

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20
Q

What is the major cytokine needed for Mast cells?
Basophils?
Eosinophils?

A

Stem cell factor and IL-3
IL-3
IL-5

21
Q

Is the expression of FcERI high or low on mast cells?
basophils?
eosinophils?

A

high
high
low

22
Q

what are the major granule contents of mast cells?

A

histamine, heparin/chondroitin sulfate, proteases

23
Q

what are the major granule contents of basophils?

A

histamine, chondroitin sulfate, protease

24
Q

what are the major granule contents of eosinophils?

A

Major basic protein, cationic protein, peroxidases, hydrolases, lysophospholipase

25
which chain of the FcERI receptor is responsible for IgE binding to activate mast cells? which chain mediates signal transduction?
alpha beta and gamma
26
Where are Abs always bound to due to the high affinity of the receptor?
receptors expressed on the cell surface
27
Biogenic amines (ie histamine) and lipid mediators (PGD2, LTC4) of activate mast cells induce what? what type of response is this?
vasodilation, vascular leak, bronchioconstriction and intestinal hypermotility immediate
28
cytokines (TNF) and lipid mediators (PAF, PGD2, LTC) contribute to what? enzymes to what? what type of response is this?
inflammation tissue damage late-phase reaction
29
what picks up allergens before migrating to LN? what happens next and what are they presented to?
DC allergens processed and presented to MHC class II
30
where are mast cells found? basophils?
in tissue in circulation
31
what does crosslinking of FcERI lead to ?
act. of cells and release of inflammatory mediators (amines, lipid mediators, chemokines and cytokines)
32
What are preformed mast cell-derived mediators?
histamine, TNF-alpha
33
What are granule associated mast cell-derived mediators?
Tryptase, chymase, peroxidase
34
What are formed during degranulation mast cell-derived mediators?
LTC4, PGD2, bradykinin, PAF
35
What are generated after transcritption mast cell-derived mediators?
IL-1, 2, 3, 4, 5, 6, GM-CSF, TNF-alpha
36
what contributes to early allergic reaction? Late?
preformed, granule associated, bradykinin LTC4, PGD2, PAF, generate after transcriptors (ILs)
37
what is essential for protection against noxious compounds, such as snake/scorpion toxins present in venoms?
mast cell proteases
38
how do mast cell proteases contribute to the inflammatory response?
degrading tight junction/hemidesmosomes, or inducing cytokine maturation
39
what cytokine contributes substantially to the pro-inflammatory response?
TNF
40
TNF-alpha and IL-1 have what target? what effect?
endothelial cells inflammation
41
what effect does PGE2 have?
pain and vascular permeability
42
what effects does bradykinin have?
vasodilator, SM contraction, vascular permeability
43
what effects does histamine have? what has the same effects as this?
SM contraction and vascular permeability PGD2 and Leukotrienes
44
what is atopy? how is it demonstrated?
the propensity for developing immediate hypersensitivity reactions to common environmental allergens by skin prick test
45
what causes chronic disease development?
activation of Th2 lymphocytes and macrophages recruitment and degranulation of eosinophils obstruction and increase in airway responsiveness progression inflammation toward airway remodeling
46
what are some things that happen in airway tissue remodeling?
activation of tissue fibroblasts, INC production of collagen and deposition INC production of mucous by Goblet cells SM hyperplasia and hypertrophy INC acute obstruction of airflow
47
what are 3 characteristics of COPD?
disrupted alveolar attachments mucous hypersecretion mucosal and peribronchial inflammation and fibrosis
48
In desensitization the presence of IgE in the blood shifts away from IgE to what?
IgG
49
what are the 3 mechanisms of desensitization?
IgG blocking Abs (IgG4 competes with IgE for allergen binding) Regulation (repeated exposure induces Tregs which invoke normal res) Immune deviation (shift away from Th2 to Th1 CD4 cells results in cytokines, ie. IFN-Gamma which are inhibitory to IgE production)