Type 1 HSRs Flashcards

1
Q

What is a type I HSR?

A

Immune reaction to innocuous/environmental antigen mediated by IgE induced degranulation

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2
Q

What are the 3 phases of type I HSRs?

A
  1. sensitization
  2. early phase
  3. late phase
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3
Q

What happens during the early phase of type I HSRs?

A

mast cell degranulation
IgE–FCERI
release of primary/secondary mediators

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4
Q

What happens during the late phase of type I HSRs?

A

cytokine production (IL-4, 5,13)
cellular recruitment (granulocytes and TH2)

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5
Q

What are 4 granulocytes?

A
  1. mast cells
  2. eosinophils
  3. neutrophils
  4. basophils
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6
Q

What receptor does IgE bind to with high affinity?

A

FCERI

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7
Q

What cytokine induces IgE class switching?

A

IL-4

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8
Q

What cytokine induces eosinophil recruitment?

A

IL-5

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9
Q

What cytokines signal to goblet cells?

A

IL-13

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10
Q

Where are mast cells located?

A

tissue

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11
Q

What is primary mediator?

A

histamine

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12
Q

What are 3 secondary mediators?

A
  1. prostaglandins
  2. leukotrienes
  3. TNF-a (anaphylaxis)
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13
Q

Degranulation induces PLA to produce ________ which makes __________ and _________

A

arachidonic acid
prostaglandins and leukotrienes

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14
Q

What pathway does leukotrienes use?

A

lipoxygenase

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15
Q

What pathway does prostaglandins use?

A

COX 2

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16
Q

What is the product of leukotriene synthesis?

A

cys LTR1

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17
Q

What is the product of prostaglandin synthesis?

A

DP1 and CRTH2

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18
Q

How does Singulair (Montelukast) reduce asthma symptoms?

A

cys-LTR1 antagonist (prevents leukotriene synthesis)

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19
Q

What does degranulation induce?

A

vasodilation
vascular permeability
smooth muscle contractions
mucus production
ROS/RNS

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20
Q

At high concentrations of NO its combined with ROS to form ____________

A

peroxynitrite

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21
Q

What 3 ways does peroxynitrite damage cells?

A

protein oxidation
apoptosis
necrosis

22
Q

What cytokine induces the transition to the late phase response and why?

A

TNF-a
induces vascular permeability and adhesion molecules

23
Q

What are some way the severity of the type I HSR can be affect?

A
  1. prior exposure
  2. concentration
  3. route of entry
  4. predisposition
24
Q

What cytokine is important for anaphylaxis and why?

A

TNF-a
induces vascular permeability and adhesion molecules = now systemic

25
Q

How does epinephrine inhibit anaphylaxis?

A

binds to alpha/beta adrenergic receptor which counter acts primary/secondary mediators
** improves cardiac output

26
Q

How do steroids inhibit inflammation?

A

blocks pro-inflammatory NFkB signaling

27
Q

What is the goal of SCITs?

A

divert the TH2 response

28
Q

What 2 mechanisms do SCITs use to reduce allergies?

A
  1. induce Tregs (IL-10) and reduce TH2 (IL-4)
  2. switch IgE to IgG (FCGRIIB)
29
Q

What is the inhibitory receptor on granulocytes used by IgG to prevent degranulation?

A

FCGRIIB

30
Q

What does SHIP Phosphatase do in SCITs?

A

prevents IgE–Lyn phosphorylation –> degranulation

31
Q

Beta-2 agonists target the same receptor as __________

A

epinephrine

32
Q

How do anticholinergics reduce asthma symptoms?

A

allows acetylcholine to bind to M2 inhibitory receptor preventing ACs normal function of airway hyper-reactivity

33
Q

What happens when eosinophils degranulate in the lungs in regards to M2 receptors?

A

MBP will bind to M2 so now acetylcholine cannot = no longer inhibitory = hyper-reactivity and bronchial spasms

34
Q

Where are type I IL-4/13 receptors found?

A

lymphocytes

35
Q

Where are type II IL-4/13 receptors found?

A

epithelial cells, goblet cells, smooth muscle cells, endothelial cells

36
Q

What’s the difference between type I and II IL-4/13 receptors besides where they are located?

A

type I only binds IL-4
type II binds IL4- and IL-13

37
Q

Atopic dermatitis is a IL-___ dominant disease

A

IL-13

38
Q

Atopic dermatitis is a TH___ mediated response

A

TH2

39
Q

What does atopic mean?

A

predisposition to allergic responses involving IgE

40
Q

What is the atopic march?

A

AD development early in life commonly leads to food allergies –> asthma —> rhinitis

41
Q

Asthma is IL-_____ dominant

A

IL-4

42
Q

What is the genetic mutation in AD?

A

FLG gene

43
Q

What does the FLG gene do?

A

crosslinks epidermal layer so its strong

44
Q

FLG mutation is common in what race?

A

europeans and asians

45
Q

What race has higher IL-17/TH17 levels in AD?

A

asians

46
Q

FLG mutation is less common in _____________ but their AD is just as severe

A

african americans

47
Q

What race has the highest IgE/Th2 response and a very low Th17/22 response?

A

african americans

48
Q

Why is it important that AD is mediated differently in different races?

A

AD is not just mediated by TH2 but also TH17 due to polymorphisms

49
Q

What is the polymorphism in AD regarding races?

A

(Q576R) IL-4 Ra gene mutatio

50
Q

What are the 3 distinct features of AD?

A

epithelial barrier dysfunction
susceptibility to infections
atopic features (rhinitis and asthma)

51
Q

What are 3 type I HSRs?

A

atopic dermatitis
asthma
allergies