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Flashcards in Immuno - Resp Deck (83):
1

What is a type I hypersensitivity?

immediate with IgE, mast cells and lipid mediators

2

What is a type IV hypersensitivity?

delayed, CD4 mediated

3

What is Atopy? or an atopic individual? 3 things are high?

high IgE
eosinophils
IL-4 secreting TH2 cells

4

Will you know you're being sensitized to an allergen?

Not necessarily, you may not even realize until next exposure

5

example of a local response to Type I hypersensitivity?

rhinitis,

6

Example of a systemic response to Type I hypersensitivity?

anaphylaxis

7

Responses to Type I hypersensitivity?

Immediate and late phase

8

are inhaled allergens lipids? sacharrides? or proteins?

protein via small carrier particles

9

are allergens usually insoluble?

usually soluble

10

You need high dose of allergen to be sensitized?

Only very low dose, like 1micro-gram per year

11

allergens are often proteins? enzymes? lipids?

enzymes

12

What's Der p 1?

dust mite faeces allergen

13

T/F? DCs produce IL-4

Nope. They produce IL-33

14

What its the role of Basophils in Type 1 hypersensitivity?

Act as an APC
secrete IL-4 either after IL-33 or allergen binding

15

What do you need for TH2 differentiation?

1. CD40 antigen binding
2. Co-stim
3. IL-4 cytokine

16

Where are mast cells usually located?

mucosal/epithelial/near blood vessels

17

Mast cells bind IgE using what?

high affinity FcER

18

What's so special about FcER on mast cells?

The only one that can bind the antibody WITHOUT it's antigen...

19

3 steps for mast cell activation

1. secretion of preformed mediators (histamines)
2. synthesis and secretion of lipid mediators (protaglandins/leukotrienes)
3. cytokine production (slow)

20

initial (0-5min) wheal and flare is soft or hard feeling?

soft feeling

21

late phase (8-12 hours) mast cell activation is soft or hard feeling?

hard feeling due to mediators

22

Allergic response is dependent on what?

Type of tissue

23

What's urticaria?

rashes/hives

24

Where and when are eosinophils usually found?

mucosal linings, found late in allergic response

25

What increases Eosinophil production in bone marrow?

IL-5 by TH2 and mast cells

26

What are eotaxins?

mediators that attract eosinophils to inflammatory site

27

increased sensitivity happens how on mast cells?

more FcEr on surface and IgE binding

28

4 treatments for allergy?

1. adrenaline (anaphylaxis)
2. B2 adrenergic receptor agonists (asthma)
3. antihistamines
4. corticosteroids

29

What does T-cell desensitization/immunotherapy tolerance mean? 4 things

Anergy
deviation of cytokines
apoptosis
Treg cells

30

What's anergy?

decreased allergen-induced proliferation

31

What kind of hypersensitivity involved T-cells/macrophages and CD8 cells?

Type IV

32

Why do you get Type IV hypersensitivity?

persistent antigenic stimulation

33

What is DTH?

Delayed type hypersensitivity

34

What happens in Delayed type hypersensitivity sensitization phase?

proliferation of TH1, helper T-cells, CD8 in lymph node, they go back to tissue and persist just waiting for next exposure

35

What does
contact sensitivity
TB
celiac disease have in common?

All are Type IV Delayed type hypersensitivity

36

Mycobacterium TB is a what kind of pathogen?

facultative intracellular pathogen

37

What's the good news with DTH and TB?

restrict 90% of growth

38

What's the bad news with DTH and TB?

small % of ppl interrupts respiratory function

39

What's a telltale sign of TB infection in lung tissue on microscope?

Granuloma: multinucleate giant cells epithelioid cells, lymphocytes

40

>90% of celiac disease ppl are what positive?

HLA-DQ2 positive

41

What does the Delayed type hypersensitivity do to the small intestine?

damages villi

42

What's the incidence of celiac disease?

1 in 70

43

Normally, does gliadin peptides bind to HLA DQ2?

poorly

44

How does glutamine --> glutamate?

via tissue transglutaminase 2 (tTg2)

45

what's an autacoid?

local mediator

46

4 things autacoids can do?

smooth muscle tone
glandular
fluid leak/oedema
sensory(pain/itch)

47

What is Cysteinyl

a Leukotriene in allergies

48

What's red man syndrome?

allergic reaction to morphine or vancomycin

49

What is a possible reason behind exercise induced bronchospasm?

increased air flow through bronchi created hypo-osmotic surface enough to trigger mast cells

50

ITAMS have no what?

intrgral kinase activity

51

Diacylglycerol protein kinase C + inositol triphosphate Ca2+ mobilisation = ??????

degranulation of mast cells

52

Once IgE is bound, it activates MAPK which does what?

arachidonic acid
cytokine gene transcription

53

Once IgE is bound, it activates phospholipase C which does what?

degranulation

54

How long does it take to cause mast cell degranulation?

30-45 seconds

55

When does mast cell activity peak?

10-30 minutes

56

4 immediate mast cell communication methods?

histamine
heparin
tryptase
TNF-a

57

2 rapid mast cell communication methods?

cys-LTs
PGD2

58

3 slow mast cell communication methods?

IL-4
IL-5
GM-CSF

59

Why are antihistamines not used in asthma?

older antihistamines were H1 receptor blockers however H1 activation will cause bronchospasm/constriction

60

What does histamine do to H2 receptors? 2 things

1. positive inotropic and chronotropic
2. Gastric acid secretion

61

H1 receptor activated by histamines does 6 things:

pain/itch
bronchospasm
mucus secretion
vasodilation
fluid leak
CNS - wakefulness

62

Should you block prostaglandins or cysteinyl leukotrienes? Why?

Leukotrienes cause it will only affect inflammation unlike prostaglandins which have lots of other effects

63

What's 5-lipoxygenase? how activated?

the inflammation bitch. It's all it does.
Activated by increased intracellular calcium

64

Where does the leukotriene receptor antagonists block LTs?

At CysLT1 receptor

65

What leukotriene attracts leukocytes?

Leukotriene B4

66

Where does Aspirin, NSAIDS Coxibs act on?

Cyclooxygenase

67

What does phospholipase A2 do?

turns acyl lipid into Arachidonic acid

68

Cytokines are slow, what are they doing? 3 things

inducing gene expression changes
structural changes
inflammatory cell infiltration

69

Which cytokines are highly regulated by glucocorticoids?

IL-1, TNF-a

70

Which cytokines are not regulated by glucocorticoids?

IL-4

71

3 things in the body that can inhibit mast cells?

PGE2 (Prostaglandins)
adrenaline
cortisol

72

What do the older mast cell inhibitors like disodium cromoglycate and nedocromil sodium cause release of?

Annexin-1 which resolves inflammation

73

What's the cons of disodium cromoglycate and nedocromil sodium

modest working
only prophylactic
topical and local effects only

74

What is omalizumab?

expensive biologic: monoclonal antibody (Anti-human IgE antibody) that binds and prevents IgE to alpha chain of FcER1

75

Can you use omalizumab in asthma?

jury's still out on that one

76

What's RIT?

rushed immunotherapy

77

I have asthma, I might take some NSAIDS/COX-2 inhibitors, cool?

NO. NO. NO. doesn't do shit in asthma or hay fever, it might provoke symptoms.

78

Crap Doc, I took aspirin for my asthma and it's getting worse! what do I do?!

I'll give you LTRA (leukotriene receptor antagonists)

79

What do glucocorticoids do?

inhibit mediator (cytokine) production in airways

80

When would you use an H1 receptor antagonist for allergies? 6 things

urticaria
atopic dermatitis
hayfever
anaphylaxis
bites/stings
motion sickness

81

When would you NOT use H1 receptor antagonist?

Asthma or colds

82

3 classes of H1 receptor antagonists

1. sedative (chlorpheniramine, promethazine)
2. non sedative but risk of ventricular arrhythmia
3. newer nonsedative (cetirizine, loratidine)

83

When are cysteinyl leukotriene receptor antagonists indicated? 2 things

1. Aspirin/exercise induced asthma
2. combined with GCS/B2 agonist