Lecture 17: IgE Flashcards Preview

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Flashcards in Lecture 17: IgE Deck (47)
1

What kind of hypersensitivity reaction is allergy?

Type 1

2

Define allergy

disease following immune response to otherwise innocuous antigen

3

Define atopy

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

4

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

True

5

What are some clinical manifestations of allergy?

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

6

What is a major post translational modification on IgE molecules?

heavy glycosylation

7

How abundant is IgE in serum?

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

8

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

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

9

What do basophils and mast cells have in common?

1) cytoplasmic stores of histamine, TNFa, and leukotrienes
2) high affinity IgE FcE receptors

10

__________ are tissue bound while ________ are mostly in the blood

mast cells; basophils

11

What are the two toxic mediators in mast cells?

1) histamine
2) heparin

12

What is the lipid meditator in mast cells?

leukotrienes

13

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

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)

14

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

MCt; MCtc

15

What is one characteristic that many allergens have in common?

contain Chitin

16

What dictates our allergic responses?

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

17

Which MHC presents allergens?

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

18

What gene(s) are responsible for allergic reactions?

A multiplicity of them! act in concert

19

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

True

20

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

enzymatic activity

21

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

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

22

What is the common route of allergens?

mucosal

23

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?)

"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

Allergic responses are dependent on what kind of responses?

Th2

25

What leads to the Th2 response?

presence of IL-4 and lack of IL-12

26

What 2 cytokines dominate the profile during IgE responses?

IL-4 and IL-13

27

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

FCeR

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

28

What is required for degranulation of mast cells and basophils?

crosslinking of IgE receptors

29

What promotes IgE class switching?

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

30

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

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

characterized by mast cells and basophils

31

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

eosinophils

32

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

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

33

What cytokine stimulates release of eosinophils from the bone marrow?

IL-5

(eotaxin chemokine also helps)

34

How does IL-5 help in the allergic response?

increases FceR display (augments IgE)

35

Which inflammatory enhancer is produced by eosinophils?

major basic protein

36

Clinical manifestations of the allergic response are dependent on what?

site of reaction

37

What is anaphylaxis and when does it come on?

immediately; bronchiolar constriction and increased vascular permeability

blood pressure plummets, heart rate rises

38

What is allergic rhinitis?

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

39

What is uticaria?

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

40

What is the hygiene hypothesis?

decreased childhood infection is increasing allergies
(worm infected children that are treated develop allergies)

41

What is the support for hygiene hypothesis?

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

42

What is the most important component in diagnosing allergies?

taking a careful history

43

What is the RAST test?

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

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

skin test

45

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

True

46

What is a common treatment for allergies?

anti-IgE

47

What is another, clever treatment to allergies?

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