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OLD "MIC 661" > Quiz 3 > Flashcards

Quiz 3 Flashcards

1
Q

What is a hypersensitivity reaction?

A

when the immune system responds inappropriately to innocuous antigens

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2
Q

What does anaphylaxis mean?

A

against protection

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3
Q

What is the recognition molecule for type I HSR?

A

IgE

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4
Q

What is the effector mechanism of type I HSR?

A

mast cell, basophil, and eosinophil degranulation

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5
Q

What are the 3 phases of type I HSR?

A
  1. sensitization phase
  2. early effector phase
  3. late phase
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6
Q

What happens during the sensitization phase of type 1 HSR?

A

first exposure to antigen

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7
Q

What happens during the early effector phase of type 1 HSR?

A

primary and secondary mediators are released and granulocytes are activated

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8
Q

When does IgE–FcERI binding happen in type 1 HSR?

A

early effector phase

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9
Q

What is the difference between primary and secondary mediators?

A

primary are stored in granules
secondary have to be synthesized

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10
Q

What happens during the late phase of type 1 HSR?

A

Th2 cells involvement
- recruit granulocytes
- increased cytokine production

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11
Q

Where are FcERI receptors found?

A

on granulocytes to induce degranulation

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12
Q

What are the steps of the early phase of type 1 HSR?

A
  1. free IgE binds to high affinity FcERI on granulocytes
  2. IgE binds to multivalent antigens
  3. IgE–FcERI interact and induce receptor clustering and signaling
  4. degranulation (primary and secondary mediators released)
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13
Q

_____ cells promote class switching of B cells to IgE

A

Th2

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14
Q

Where does somatic hypermutation occur on an antibody? What about isotype switching?

A

somatic: Fab region
isotype switching: Fc region (bottom)

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15
Q

What cytokine promotes IgE class switching?

A

IL-4/13

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16
Q

IgE has an unique 3 domain ____ region

A

Fc

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17
Q

What Ig has the same 3 Fc domain but is pentameric?

A

IgM

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18
Q

What part of IgE binds to the FcERI?

A

Fc region

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19
Q

Ig___ is low in the serum compared to other Igs

A

IgE

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20
Q

Where are mast cells found?

A

tissue (final epithelial layer)

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21
Q

Where are basophils found?

A

blood

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22
Q

Where are eosinophils found?

A

blood (migrate to tissue)

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23
Q

What phase of type I HRS are eosinophils and neutrophils the most important?

A

late phase

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24
Q

What molecules does IgE bind to?

A

proteins or glycoproteins

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25
Q

What is the IgE signaling cascade?

A
  1. allergen binds to IgE which is bound to FcERI
  2. FcEREI clusters = activation of Lyn tyrosine kinase
  3. Lyn phosphorylates ITAMs
  4. Syk recruits SH2 to ITAMS
  5. Syk is autophosphorylated = activation of PLC-gamma
  6. degranulation, PLA activation, cytokine production.
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26
Q

What is the result of the IgE signaling cascade?

A

degranulation
PLA (phospholipase A) activation
cytokine production

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27
Q

What phase of type 1 HSR do primary and secondary mediators play a role?

A

early phase

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28
Q

What are primary mediators derived from?

A

decarboxylated histidine

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29
Q

How many histamine receptors do cells have?

A

4

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30
Q

Which histamine receptor do anti-histamines target?

A

H1

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31
Q

Binding of H1 (histamine) receptor induces what?

A

smooth muscle contractions
increased vascular permeability
mucus

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32
Q

Binding of H2 (histamine) receptor induces what?

A

increased vascular permeability
vasodilation
release of acid into stomach

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33
Q

What are 2 examples of primary mediators?

A

histamine
heparin

34
Q

Degranulation of secondary mediators is induced by ________ that generates ________ to produce leukotrienes and prostaglandins

A

phospholipase A2
arachidonic acid

35
Q

What are 3 examples of secondary mediators?

A
  1. leukotrienes
  2. prostaglandins
  3. IL-1/TNF-a
36
Q

What enzyme pathway synthesizes leukotrienes?

A

lipoxygenase

37
Q

What enzyme pathway synthesizes prostaglandins?

A

COX2

38
Q

What are the steps of the leukotriene synthesis pathway?

A
  1. cPLA2 +membrane phospholipids
  2. AA (arachidonic acid)
  3. LOX
  4. Cys LTR1(receptors)
39
Q

What are the steps of the prostaglandin synthesis pathway?

A
  1. PLA2 +membrane phospholipids
  2. AA (arachidonic acid)
  3. COX 1&2
  4. DP1 & CRTH2 (receptors)
40
Q

What is TNF-a?

A

inflammatory cytokine

41
Q

Where is TNF-a stored?

A

mast cell granules

42
Q

What does expression of TNF-a increase?

A

selectin and integrins
permeability
vasodilation

43
Q

What do eosinophils release to kill pathogen?

A

MBP (major basic protein)
-reactive O2 species

44
Q

What do neutrophils release to kill pathogen?

A

MPO (myeloperoxidase)
-reactive O2 species

45
Q

What are the steps to making a reactive oxygen species?

A
  1. O2
    add NADPH oxidase
  2. super oxide anion
    add superoxide dismutase
  3. hydrogen peroxide
    add myeloperoxidase
    hypochlorous acid
46
Q

What are the steps to making a reactive nitrogen species?

A
  1. L-arginine
    add inducible nitric oxide synthease (iNOS)
  2. nitric oxide
  3. nitrogen dioxide
47
Q

When there is a high concentration of NO (reactive nitrogen species) what happens?

A

it combines with the (ROS) superoxide anion and produces peroxynitrite

48
Q

When there is a low concentration of NO (reactive nitrogen species) what happens?

A

its a signaling molecule

49
Q

What are the affects of peroxynitrite?

A

inactivation of mitochondria = apoptosis
protein oxidation (cysteine) = inactive enzyme
DNA damage = necrosis

50
Q

What induces iNOS?

A

inflammatory Th2 cytokines
epithelial cell damage

51
Q

What is a systemic reaction of a type 1 HSR?

A

anaphylaxis

52
Q

What is a localized reaction of a type 1 HSR?

A

hives
asthma

53
Q

The severity of clinical symptoms of type 1 HSR depends on what 4 things?

A
  1. route of allergen
  2. concentration of allergen
  3. prior exposure to allergen
  4. host pre-disposition
54
Q

What does epinephrine bind to to prevent anaphylaxis?

A

(g-protein coupled receptor) alpha and beta adrenergic receptors

55
Q

What does epinephrine block by binding to the adrenergic receptors?

A

primary and secondary mediators being released from granulocytes

56
Q

Whats an example of a leukotriene antagonist?

A

Singulair

57
Q

What 4 things do corticosteroids do?

A
  1. decrease inflammation: blocking inflammatory mediators
  2. immunosupressive: suppresses T cells
  3. anti-proliferative: inhibit epidermal cell turnover
  4. vasoconstrictive: inhibit histamine
58
Q

What does glucocorticoid steroids inhibit?

A

NfkB nuclear factor (so it cannot enter nucleus and turn on inflammation genes)

59
Q

All pattern recognition receptors activate _______

A

NfkB

60
Q

Subcutaneous immunotherapy (SCITs) are a type of ____sentization therapy

A

hyposentization

61
Q

What is the main goal of SCITs to prevent an immune response?

A

divert Th2 response from pathogenic to tolerant

62
Q

How do SCITs divert the Th2 response?

A

T cells are redirected to produce Tregs instead of Th2 (IgE–>IgG)

63
Q

What are the steps of SCITs inhibiting an immune response?

A
  1. induce IL-10 production (increase T regs and decrease Th2)
  2. IgE shifts to IgG
  3. IgG binds to FcGRIIB (inhibitory FcERI)
  4. no degranulation
64
Q

IL-4 promotes _____ class switching

A

IgE

65
Q

IL-10 promotes ______ class switching

A

IgG

66
Q

What is FcGRIIB?

A

inhibitory version of FcERI

67
Q

Does FcGRIIB use ITAMs or ITIMS?

A

ITIMs

68
Q

How is FcGRIIB inhibitory?

A

prevents Lyn phosphorylation

69
Q

Beta-2 agonists target the same receptor as ____________

A

epinepherine

70
Q

What does SHIP phosphatase do for FcGRIIB?

A

removes phosphate from ITAMs to inactivate them

71
Q

What is the mechanism of anti-IgE therapy?

A

bind to IgE and prevents it from binding to FcERI

72
Q

What is the mechanism of anti-IL13 therapy?

A

blocks IL-13 or its receptor
- doesnt work very well because IL-4 picks up the pace

73
Q

What is the mechanism of IL-4Ra therapy?

A

blocks IL-4Ra receptor because IL-13 or IL-4 both use it
- worked

74
Q

What is the mechanism of anti-IL4 AMG317 therapy?

A

blocks IL-4Ra receptor because IL-13 or IL-4 both use it
- doesn’t work well because its outcompeted

75
Q

What is the mechanism of anti-TSLP therapy?

A

prevent CD4 cells turning into Th2

76
Q

What is the mechanism of anti-IL5Ra therapy?

A

blocks IL-5 receptor and induces AMCT

77
Q

How does Singulair (Montelukast) prevent asthma symptoms?

A

prevents leukotriene pathway by blocking cysLTR1 (cys-LT antagonist) cys-leuoktrienes

78
Q

What does FEV stand for?

A

forced expiratory volume (amount)

79
Q

What is PEF stand for?

A

peak expiratory flow (speed)

80
Q

_________ increases cardiac output (higher BP and more blood flow, dilated veins)

A

epinephrine

81
Q

What cytokine initiates the transition to the late phase response?

A

TNF-a

OLD "MIC 661" (19 decks)

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