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MICR2221 - Medical Immunology > L5 - Hypersensitivity > Flashcards

L5 - Hypersensitivity Flashcards

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USMLE® Step 1 flashcards
1
Q

What is a type I allergic reaction?

A

IgE-mediated
30 mins

e.g. allergic asthma

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2
Q

What is type II allergic reaction?

A

Cytotoxic reaction
days
IgG-mediated
e.g. drug allergy

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3
Q

What is type III allergic reaction?

A

Immune complex reaction
6-8h
IgG-mediated

e.g. allergic vasculitis

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4
Q

What is type IV allergic reaction?

A

T-cell mediated
28-72h
Th1/Th2/CTL-mediated

e.g. allergic contact eczema

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5
Q

What are general properties of allergens?

A

small
soluble
proteases
long lasting

mostly promote type-II response

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6
Q

Descrive protease mediated Type-1-IgE hypersensitivity

A

enzyme: Der p 1

cleaves occludin in tight junction

enters mucosa

dendritic cel primes in lymph node

Plasma cell travels back to mucosa

produce Der p 1-specific IgE antibodies

Der p 1-specific IgE binds to mast cell

triggers mast cell degranulation

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7
Q

What allergic responses can mast cells mediate?

A

oedema swelling
peristalsis
snotty nose
increase blood flow

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8
Q

What are IgE-mediated diseases?

A

systemic anaphylaxis

acute urticaria

hay fever

asthma

food allergy

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9
Q

What is IgE mediated reaction to inhaled allergen in the UPPER AIRWAYS?

A

rhinitis

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10
Q

What is IgE mediated reaction to inhaled allergens in the LOWER AIRWAYS?

A

Asthma

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11
Q

What reponse is T-bet crucial for?

A

Th1

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12
Q

What happens when you create a T-bet knockout?

A

get a Th2 response (Th1 usually inhibits Th2 response)

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13
Q

What happens during urticaria/anaphylaxis?

A

MAJOR lowering of blood pressure

airway constriction

swelling epiglottis

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14
Q

What is vibrational urticaria?

A

overly sensitive mechanotransduction = mast cell DEGRANULATION

OVER ACTIVATION OF GPCR - EMR2

mutations make receptor susceptible to lose N-terminus

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15
Q

How can allergic reaction be diagnosed

A

In vivo

in vitro - specific IgE, ELISA

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16
Q

What did the IgE response originally evolve to do?

A

expel/destroy helminth/protozoal pathogens

17
Q

Why is allergy on the increase?

A

Th1 inflammatory immune defects rising

changes to clean environment in developing countries skews immune response to Th2

18
Q

What is atopic dermatitis?

A

chronic inflammation

apoptosis of keratinocytes

Leaky skin binds keratin fibres together

19
Q

What is Type II hypersensitivity?

A

Ig or IgM bind to cell surface Ab:

  • activating complement
  • bind Fc receptors on Tc and Nk cells - promote ADCC

lysis of Ab-coated cell

20
Q

What are clinical examples of Type II responses?

A

Grave’ disease
- thyroid

Myasthenia Gravis
- Ach receptors

haemolytic anaemia

21
Q

What are Type III diseases?

A

IgG immune complex deposition on vessel walls = Arthus reaction

Immune complex-mediated cytotoxicity

MOST DAMAGE STEMS FROM ACTIVITY OF NEUTROPHILS - difficult for neutrophils to phagocytose, still release LYTIC ENZYMES

22
Q

What is Type IV hypersensitivity?

A

delayed hypersensitivity

23
Q

What is allergic contact dermatitis?

A

Th1 cell mediated

Mediated via lipid soluble urushiol oil haptens binding MHCI - poison ivy complex

24
Q

What is Coeliac disease?

A

villous atrophy

crypt hyperplasia

25
Q

What is the allele that 95% of coeliac patients have?

A

HLA-DQ2 class II MHC allele

binds a-gliadin

26
Q

What cellular destruction occurs in coeliac disease?

A

peptides produced from gluten do not bind MHC class II

enzyme tTg modifies peptide so they bind

peptide binds & activates gluten-specific CD4 T cells

activated R cells kill mucosal epithelial cells - binds Fas & also secrete IFN-y

27
Q

Why does the cellular destruction of coeliac disease not happen with multiple food proteins?

A

protease resistant peptides may cause increase in IL-15 - induces NKG2D-ligands

increase intraepithelial lymphocyte mediated killing

MICR2221 - Medical Immunology (16 decks)

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