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Host Defense > Lecture 17: IgE > Flashcards

Lecture 17: IgE Flashcards

1
Q

What kind of hypersensitivity reaction is allergy?

A

Type 1

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2
Q

Define allergy

A

disease following immune response to otherwise innocuous antigen

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3
Q

Define atopy

A

The ability to transfer reactivity to allergens by means of serum (aka the ability to make IgE)

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4
Q

True or false: allergic reactions have double in the past 10-15 years

A

True

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5
Q

What are some clinical manifestations of allergy?

A

smooth muscle spasm
increased vascular permeability
activation of inflammatory and coagulation cascades

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6
Q

What is a major post translational modification on IgE molecules?

A

heavy glycosylation

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7
Q

How abundant is IgE in serum?

A

usually VERY LOW concentrations (it is a cell bound antibody found mainly at host-environmental interfaces)

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8
Q

Where are the binding sites for FcERs? (what cells have them)

A

mast cells and basophils (and on APCs at much lower levels)

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9
Q

What do basophils and mast cells have in common?

A

1) cytoplasmic stores of histamine, TNFa, and leukotrienes

2) high affinity IgE FcE receptors

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10
Q

__________ are tissue bound while ________ are mostly in the blood

A

mast cells; basophils

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11
Q

What are the two toxic mediators in mast cells?

A

1) histamine

2) heparin

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12
Q

What is the lipid meditator in mast cells?

A

leukotrienes

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13
Q

What distinguishing feature divides the two major subtypes of mast cells?

A

what enzymes are expressed

MCt = tryptase
MCtc = tryptase and chymase

(but since both have tryptase, tryptase staining is the primary way to identify mast cells)

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14
Q

____ are the primary mast cells of the mucosa while _____ are in the connective tissue like skin

A

MCt; MCtc

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15
Q

What is one characteristic that many allergens have in common?

A

contain Chitin

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16
Q

What dictates our allergic responses?

A

our genes (50% of children from 2 atopic parents will be atopic)

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17
Q

Which MHC presents allergens?

A

2 (D class perhaps promotes IgE production over IgG by influencing the type of TLR activated)

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18
Q

What gene(s) are responsible for allergic reactions?

A

A multiplicity of them! act in concert

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19
Q

True or false: there is a direct relationship between serum IgE levels, allergic reactions and the atopic state

A

True

20
Q

Almost anything can be an allergen but what heightens the probability that our immune system will mount a response?

A

enzymatic activity

21
Q

What is one big reason for why timing is important in the allergic response?

A

decreased early exposure to infections in genetically predisposed individuals is associated with insufficient Treg control of IgE

22
Q

What is the common route of allergens?

A

mucosal

23
Q

How does the body know if it is taking up allergen or actual pathogen? (in other words, what pushes the processing towards the IgE route vs the IgG?)

A

“allergic” TLRs that induce DC to produce IL-4 instead of IL-12 (Th2 instead of normal Th1)

also, presentation of peptide as well as the nature of it shift it towards the dominant IgE

24
Q

Allergic responses are dependent on what kind of responses?

A

Th2

25
Q

What leads to the Th2 response?

A

presence of IL-4 and lack of IL-12

26
Q

What 2 cytokines dominate the profile during IgE responses?

A

IL-4 and IL-13

27
Q

What is the ONLY receprot that can be occupied without antigen?

A

FCeR

Fc receptor for IgE wants to bind empty IgE - then the cell is armed and ready

28
Q

What is required for degranulation of mast cells and basophils?

A

crosslinking of IgE receptors

29
Q

What promotes IgE class switching?

A

upregulation of CD23 on mast cells and basophils that increase their production of IL-4 and 13

30
Q

What happens within the first 15 minutes (immediate reaction) of an allergic reaction?

A

prostaglandin and leukotriene release; direct complement activation by tryptase (BUT YOU NEED PRIOR EXPOSURE)

characterized by mast cells and basophils

31
Q

What is the late phase (slow-acting - takes hours) of an allergic reaction characterized by?

A

eosinophils

32
Q

The late phase is completely dependent on T cell activation as well as which cytokines?

A

IL-3, 4, 5, 13, TNFa, GM-CSF, IL-10

33
Q

What cytokine stimulates release of eosinophils from the bone marrow?

A

IL-5

eotaxin chemokine also helps

34
Q

How does IL-5 help in the allergic response?

A

increases FceR display (augments IgE)

35
Q

Which inflammatory enhancer is produced by eosinophils?

A

major basic protein

36
Q

Clinical manifestations of the allergic response are dependent on what?

A

site of reaction

37
Q

What is anaphylaxis and when does it come on?

A

immediately; bronchiolar constriction and increased vascular permeability

blood pressure plummets, heart rate rises

38
Q

What is allergic rhinitis?

A

occurs when allergen binds to cells in the nasal submucosa and incites chronic allergic reaction

39
Q

What is uticaria?

A

hives (occur when IgE armed mast cells are activated in the skin)

40
Q

What is the hygiene hypothesis?

A

decreased childhood infection is increasing allergies

worm infected children that are treated develop allergies

41
Q

What is the support for hygiene hypothesis?

A

evidence that early exposure to childhood illness sets normal Th1 and Th2 responses to subsequent environmental antigen exposure

42
Q

What is the most important component in diagnosing allergies?

A

taking a careful history

43
Q

What is the RAST test?

A

Radio Allergo Sorbent Test

add patient serum to cellulose disc with allergen, if IgE is present in the serum, it will bind. After washing, add radio labeled anti-IgE then count with a gamma counter

44
Q

In addition to RAST, what other test can you do?

A

skin test

45
Q

True or false: diagnostic tests are only used as adjunct to clinical symptoms

A

True

46
Q

What is a common treatment for allergies?

A

anti-IgE

47
Q

What is another, clever treatment to allergies?

A

allergen immunotherapy (reroute IgE response by administering allergen antigens that promote Th1 response to culminate in IgG production (blocking antibodies))

Host Defense (21 decks)

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