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3rd Year Biomed > Immunology (Liz - Hypersensitivity) > Flashcards

Immunology (Liz - Hypersensitivity) Flashcards

1
Q

What is hypersensitivity?

A

Unfavourable exaggerated action of the immune response

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2
Q

What are the 4 types of hypersensitivity?

A

Type I - IgE-mediated hypersensitivity

Type II - IgG or IgM mediated cytotoxic hypersensitivity

Type III - Immune complex mediated hypersensitivity

Type IV - Cell-mediated hypersensitivity

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3
Q

What is are the typical manifestations of type I hypersensitivity?

A

Systemic and localised anaphylaxis such as hay fever, asthma, hives, food allergies and eczema

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4
Q

What is the structure of the IgE antibody?

A
  • Has an extra constant region domain (CH4) like IgM but no hinge region
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5
Q

What does IgE bind to?

A
  • Fc receptors on the membranes of blood borne basophils and tissue mast cells in the CH3 domain of the IgE molecule (look at slide 5 for clarification)
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6
Q

Describe both the first and subsequent allergic response to ragweed pollen

A

First contact:

  • Ragweed antigen binds to B cells
  • B cell differentiates to a plasma cell that produces large amounts of ragweed IgE antibody
  • IgE molecules attach to mast cells

Subsequent contact:

  • IgE-primed mast cells release molecules that cause sneezing, runny nose, watery eyes etc
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7
Q

Describe how IgE antibodies bind to the mast cell and what this triggers the mast cell to do

A
  • Bind to alpha chain of high affinity Fc receptors Fc(epsilon)RI on mast cell
  • Activated mast cells secretes IL-4 which causes B cells to class switch
  • B cells start to produce antigen-specific IgE instead of IgG
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8
Q

Which part of the FcR causes signal transduction?

A

The gamma and beta chains

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9
Q

What signal transduction occurs as a result of IgE/FcR binding?

A
  • First, activation of tyrosine kinases
  • Tyrosine kinases activate both protein kinase C (PKC) and mitogen-activated protein kinases (MAPK)
  • Both activate transcription factors such as NFkB that regulate cytokine production (e.g IL-4)
  • PKC activates phospholipase D (PLD) which causes degranulation
  • MAPK activates phospholipase A (PLA) which causes production of leukotrienes and prostaglandins

(See diagram for clarification)

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10
Q

Why are leukotrienes and protaglandins important?

A

Lipid mediators of inflammation

- cause vasodilation and increased vascular permeability

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11
Q

What is the wheal and flare reaction?

A

The reaction to allergins injected into the skin, in which blanched wheals appear surrounded by redness

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12
Q

How are people tested for whether they’re allergic to particular allergens (grass etc)

A

Intradermal injection of allergen

- Measure weal diameter 15-30 mins after exposure

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13
Q

In tern of food allergies, what is the response in nonallergic individuals vs allergic individuals

A

Nonallergic individuals:

  • Food allergens cross the gut epithelium and are taken up into APCs
  • APCs present food antigen to T cells and induce tolerance via the production of T reg cells

Allergic individuals:

  • Allergic individuals have larger gaps between intestinal epithelial cells
  • Once present, food allergen-specific IgE antibodies help transcellular food uptake via low affinity binding to CD23 on epithelial surface
  • Allergen taken in by APC
  • APC causes production of Th2 cells that signal (via cytokines e.g IL-4) to B cells to produce IgE antibodies
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14
Q

What factor influences Treg vs Th2 induction pathways

A

The gut microflora

- TLRs on APCs binding to PAMPs can induce Treg formation over Th2

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15
Q

What is the hygiene hypothesis?

A

That exposure to pets and farmyard animals etc in childhood can protect children from food allergies

  • due to early exposure to microbes
  • Drives the immune system into a general state of Th1 responsiveness and no allergy development
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16
Q

Allergic responses to inhaled antigens e.g grass pollen can be divided into what 2 phases?

A

1) Intermediate phase

2) Late phase

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17
Q

What is an asthmatic response measured using?

A

Peak expiratory flow rate (PEFR)

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18
Q

What occurs to PEFR during an asthmatic response and why?

A

Falls

  • Due to rapid histamine release from mast cells
  • Causes smooth muscle contraction
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19
Q

Describe what causes the intermediate and late phase responses and when each happens

A

Intermediate:

  • happens minutes after antigen inhalation and subsides after an hour
  • Due to mast cells releasing histamine

Late:

  • 6-8 hours after antigen challenge
  • Response in the lung
  • Due to migration of inflammatory leukocytes to the lungs attracted by chemokines
20
Q

How do dust mite fecel pellet allergens penetrate the epithelial barrier?

A

Have a proteolytic enzyme, Der p1, that cleaves occludin, a protein that helps maintain tight junctions

21
Q

How does the dust mite allergic response occur?

A
  • Der p1 taken up by dendritic cells for antigen presentation and Th2 priming
  • DC migrates to lymph node and primes naive T cell to become Th2 cell
  • Th2 cell incudes B-cell switch to IgE production
  • Plasma cell tavels back to mucosa and produces Der p1-specific IgE antibodies which bind to mast cells
  • Mast cell degranulation = allergic symptoms
22
Q

Development of atopic allergic diseases is a result of what 2 factors?

A
  • Genetic susceptibility

- Environment

23
Q

Describe the interaction between genetics and environment that give and no not give allergic responses

A

Atopic:
HIGH genetic susceptibility with ‘HYGIENIC’ environment - gives mainly Th2 responses

Non-atopic:
LOW genetic susceptibility with ‘LESS HYGIENIC’ environment gives Th1 responsiveness

24
Q

Almost all allergy triggers are from what type of organism?

A

Eukaryotic (plants,animals, fungi)

Only 1% from bacteria

25
Q

Summarise type II hypersensitivity

A
  • Induced by IgG and IgM antibodies
  • Targeted to extracellular matrix antigens or cell membranes
  • Antibody is then bound by neutrophils, eosinophils, NK cells and macrophages via their Fc receptors
  • This leads to antibody-dependant cytotoxicity (ADCC)
26
Q

Give an example disease caused by a type II sensitivity reaction

A

Haemolytic anaemia

27
Q

Where is the damage directed in type II hypersensitivity?

A

To the cell or basement membranes

28
Q

By what process do neutrophils attack basement membranes in type II sensitivity?

A

‘Frustrated phagocytosis’

  • Neutrophil adherence
  • Frustrated phagocytosis
  • Extracellular enzyme release causing damage
29
Q

By what 2 ways can neutrophils, eosinophils and macrophages bind to the basement membrane?

A
  • Fc receptor mediated
    > binding to IgG antibody
  • C3-receptor mediated
    > Binding to C3b on cell surface
30
Q

Describe how NK cells damage body cells via antibody-dependant cytotoxicity in type II hypersensitivity reactions

A

1) Antibody binds antigens on target cell surface
2) Fc receptors on NK cells recognise bound antibodies
3) Cross-linking of Fc receptors signals NK cell to kill target
4) Cell dies by apoptosis

31
Q

What is Erythroblastosis fetalis?

A

A heamolytic disease of newborns

  • Antibody-dependent cell lysis of Rhesus +ve red blood cells in foetus of a Rhesus -ve mother
32
Q

How is this disease prevented?

A

Treating the mother with rhogam

- Prevents B cell activation and memory cell formation

33
Q

What are type III hypersensitivity reactions a result of?

A

Formation of large and long-lasting antibody-antigen ‘immune complexes’ which fail to get broken down by complement and phagocytosis

34
Q

Where do these complexes accumulate ?

A

1) Kidney glomerulus (glomerulonephritis)

2) Blood vessel walls
(vasculitis)

3) Synovial membrane of joints (rheumatoid arthritis)

4) Lungs
(asthma)

35
Q

Name some examples of type III disease states

A

1) Rheumatoid arthritis
2) Systemic lupus erythrematosus
3) ‘Farmers lung’ (reaction to aspergillus leading to permanent lung damage)
4) ‘Pigeon-fanciers disease’ (reaction to avian proteins leading to inflammation of lung alveoli)

36
Q

How do type III immune complexes cause vasculitis?

A

1) Immune complexes induce platelet aggregation and complement activation
2) Platelets forms microthrombus, complement causes neutrophil activation
3) Neutrophils cannot ingest large complexes so release lysosomal enzymes externally
4) Enzymes cause damage to wall of blood vessel

37
Q

What are the characteristics of type IV hypersensitivity?

A
  • Does not involve antibody formation
  • Entirely T cell controlled
  • Macrophages and cytotoxic T cells cause tissue damage over a long time
38
Q

What are the 3 types of type IV hypersensitivity?

A

1) Contact sensitivity e.g latex
2) Delayed type (e.g granuloma formation in tuberculosis)
3) Gluten sensitivity (e.g Coeliac disease)

39
Q

What is the antigen of gluten sensitive type IV hypersensitivity?

A

Gliadin

40
Q

Describe the delayed type hypersensitivity response

A

1) Antigen processed by tissue macrophages and stimulates Th1 cells
2) Chemokines and IFN-gamma recruit macrophages to site
3) TNF-alpha and lymphotoxin secreted and cause local tissue destruction
4) IL-3 secreted stimulates monocyte production by bone marrow stem cells

41
Q

Describe the process of contact hypersensitivity to poison oak

A
  • Poison oak antigen complexed to skin and taken up by Langerhans cells and DCs
  • Langerhans cells process and present antigen on MHC class II
  • Th1 cells bind and become sensitised: secrete cytokines such as IFN-gamma, chemotactic protein (MCP-1) and migration inhibition factor (MIF)
  • These cytokines causes tissue damage (blistering) by inducing lytic enzyme release from macrophages
42
Q

What is a granuloma and why do they form?

A
  • A central core of infected macrophages
  • May include multinucleate giant cells
  • Core surrounded by CD4 positive Th1 cells
  • Core normally becomes necrotic but mycobacteria can continue to live

Occurs when mycobacteria resist the effects of macrophage activation

43
Q

What is the result of a granuloma?

A

Extensive tissue damage due to lytic enzyme release from active macrophages

44
Q

Describe the development of coeliac disease

A

1) Gluten polypeptides de-aminated by transglutaminase (tTG)
2) Allows peptides to bind to HLA-DQ2 (MHC class II)
3) MHC class II/peptide complexes presented on surfave of tTG-rective B cells and DCs
4) Peptide presentation activates Th cells to produce IFN-gamma

5) Cytokine causes severe inflammation of upper small intestine
- intestinal villi are lost
- oral tolerance to alpha-gliadin permanently lost

45
Q

What must individuals with Coeliac disease avoid?

A

Wheat, oats, barley etc

46
Q

What is a potential consequence of coeliac disease?

A

Malabsorption and diarrhoea

3rd Year Biomed (44 decks)

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