lecture 4- hypersensitivity type I

Question 1

what are allergens?

Answer 1

harmless substances that immune responses overreact to
inhaled: pollen, dust mite
injected: wasp, drugs
ingested: food
contacted: plants

Question 2

Type I, II & III are ___ reactions
Type IV is a ___ reaction

Answer 2

antibody-induced
T cell-induced

Question 3

antibodies involved with type I, II & III

Answer 3

I = IgE
II & III = IgG

Question 4

describe type I hypersensitivty

Answer 4

aka IgE-mediated hypersensitivity
- results from antigen binding to antigen-specific IgE which is bound to its FcR (FcE) on mast cells - mast cells degranulate and release inflammatory mediators, histamine
- can vary in severity from runny nose to death by asphyxiation
- aka immediate hypersensitivity (mins to hrs)
- caused by inhaled antigens like pollen

Question 5

what cell is at the heart of type I hypersensitivity response

Answer 5

mast cell- IgE already bound to mass cell surface by FcE receptor – cells ready to degranulate if cross-linked by antigens

Question 6

are you born with allergies?

Answer 6

no- develop after exposed and sensitized
- exposure – Th2 response – produces IL-4 – stimulates B cell response – isotype switching to IgE – IgE binding to mast cell by FcE – ready to degranulate later when exposed again

Question 7

describe a few IgE-mediated allergic reactions

Answer 7

1- systemic anaphylaxis - eaten or spread through circulation – causes increased vascular permeability which needs immediate attention
2- wheal & flare (redness & swelling) - localized- minimizes severity
3- allergic rhinitis/bronchial asthma - mostly localized
4- food allergy - gateway to systemic response

Question 8

describe diagnosis of case study K

Answer 8

allergic rhinitis- seasonal allergies (seasonal b/c plants)
- diagnostic testing: skin test - histamine is positive control, also need negative control
. serum specific IgE testing used when skin test cant be used

Question 9

describe early and late phase reactions

Answer 9

early phase = wheal(swelling) & flare(redness) - due to immediate mast cell degranulation

late phase = generalized swelling spreading out from initial site of exposure - due to leukotrienes, cytokines, and chemokines produced by mast cells after initial degranulation

Question 10

does early or late phase require mast cells to synthesize new immunomodulatory proteins?

Answer 10

late

Question 11

toxic inflammatory mediator functions produced by mast cells

Answer 11

histamine and herparin (present in pre-formed granules)
- toxic to parasites, increase vascular permeability, cause smooth muscle contraction

Question 12

how to treat patient K case study

Answer 12

• avoidance
• antihistamines
• immunotherapy
  . initial increase in IgE but longterm decrease in IgE
  . SHIFT IN TH1/TH2 RESPONSE - want to favor Th1 to inhibit Th2

Question 13

effects of IgE-mediated allergic responses vary with site of mast cell activation

Answer 13

GI tract- expulsion
airways- expulsison
blood vessels - edema, inflammation

Question 14

case study 2- J

Answer 14

peanut allergy- this is his second exposure b/c swelled
- systemic anaphylaxis
- serum testing showed high specific IgE level
solution- epinephrine

Question 15

if you could engineer a T cell response to inhibit type I hypersensitivity, which Th subset?

Answer 15

Th1 or Treg