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Immunology and Haematology > Hypersensitivity 2 > Flashcards

Hypersensitivity 2 Flashcards

1
Q

What immunoglobulins mediate type II hypersensitivity?

A

Mediated by IgG or IgM reacting with antigen present on surface of cell:

  • Bound IgG then interacts with complement or with Fc receptor on macrophages
  • Causing opsonisation of target cells (more susceptible to phagocytosis)
  • Take several hours
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2
Q

What are the different effects that type II hypersensitivity can cause?

A
  • Damage to red cells
    • Haemolysis
  • Damage to solid tissues
  • Functional effects
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3
Q

What are examples of type II hypersensitivity?

A
  • Immune mediated haemolysis, such as autoimmune haemolytic anaemia
  • Destruction of solid tissues, such as Goodpasture syndrome
  • Affects function, such as Graves disease
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4
Q

What are the different variations of blood type?

A
  • Rhesus positive or negative
  • I positive or negative
  • Group A, B or O
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5
Q

What is a consequence of A and B blood group antigens being oligosaccharides which are similar to molecule exposed by bacteria?

A
  • So have naturally occurring antibodies that recognise them unless we are same blood group
    • People who are group O have antibodies against both A and B
    • People who are AB have antigens against neither
    • Anti-A and Anti-B are IgM antibodies
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6
Q

People who are group O have antibodies against what groups?

A

A and B

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7
Q

People who are group AB have antibodies against what groups?

A

None

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8
Q

What type of antibodies are anti-A and anti-B?

A

IgM antibodies

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9
Q

What is unique about IgM?

A

IgM antibodies are multivariant (can combine to multiple antigens)

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10
Q

What is a complication of IgM being multivariant?

A

IgM antibodies are multivariant (can combine to multiple antigens):

  1. Causes agglutinate of red blood cells
  2. IgM activates complement and the membrane attack complex destroying RBC
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11
Q

How does IgG lead to destruction of red cells?

A

IgG does not damage circulating red cells:

  1. Fc receptors on splenic macrophages bind IgG coated red cells, which are then destroyed
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12
Q

What can autoimmune haemolysis occur due to?

A
  • Rhesus antigen (IgG develops during pregnancy and crosses the placenta and causes haemolytic disease
  • Incompatibility in the ABO system during blood transfusion
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13
Q

What can autoimmune haemolytic anaemia be caused by?

A
  • Induced by infections or drugs
  • Part of systematic autoimmune disease (SLE)
  • Autoantibodies produced by malignant B cells
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14
Q

Describe the pathophysiology of Goodpasture syndrome?

A
  1. IgG autoantibodies bind a glycoprotein in basement membrane of lung and glomeruli
  2. Anti-basement membrane antibody activates complement, triggering inflammatory response
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15
Q

Describe the genetics of Graves disease?

A
  • Family history
  • HLA allele DR3
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16
Q

Describe the epidemiology of Graves disease?

A
  • Most common cause of hyperthyroidism
  • Young woman
17
Q

Describe the pathophysiology of Graves disease?

A
  • Thyroid stimulated with an autoantibody that binds into the THS receptors, causing thyroxine secretion
18
Q

What is type III hypersensitivity?

A
  • IgG responsible
  • Immune complexes of antigen and antibody form and cause damage at site of production or circulate and cause damage elsewhere
  • Take time to form and initiate tissue damage
19
Q

What Ig mediates type III hypersensitivty?

A

IgG

20
Q
A
21
Q

Antigens that form complexes must be what?

A
  • Polyvalent
  • Present long enough to start an antibody response
22
Q

Why is the antigen:antibody ratio important for type III hypersensitivity?

A
  • At low levels of antibody, each antigen binds several immunoglobulin molecules
  • When antibody and antigen levels are equal, or antibody in slight excess, large complexes can form
  • When antibody exceeds antigen small complexes form
23
Q

When do small and when do large complexes form?

A
  • When antibody and antigen levels are equal, or antibody in slight excess, large complexes can form
  • When antibody exceeds antigen small complexes form
24
Q

Describe the process of clearing complexes?

A
  1. Done by compliment system
  2. Complement receptor 1 (CR1) transfers complexes to phagocytes
25
Q

What does failure of clearance of complexes lead to?

A

Failure of clearance leads to immune complex disease:

  • Activation of innate immune system
26
Q

What are two diseases type III hypersensitivty is involved in?

A

Glomerulonephritis

Farmer’s lung

27
Q

What is the presentation of glomerulonephritis due to hypersensitivity?

A
  • Nephrotic syndrome (protein leaks into urine) with gradual development of renal failure
  • Nephritis with rapid onset renal failure, blood and protein in the urine and hypertension
28
Q

What is Farmer’s lung?

A

Hypersensitivity reaction to fungal spores:

  1. Precipitating IgG antibodies against mold proteins
  2. If patient inhales mold protein, insoluble immune complexes form in lung tissues
29
Q

What is type IV hypersensitivity?

A

Delayed hypersensitivity reaction:

  • Mediated by T cells
  • Takes 2-3 days to develop
30
Q

What mediates type IV hypersensitivity?

A

T cells

31
Q

How long is the onset of type IV hypersensitivity?

A
  • Takes 2-3 days to develop
32
Q

What are the main diseases of type IV hypersensitivity?

A
  • Rheumatoid arthritis
  • Multiple sclerosis
33
Q

Describe the mechanism of type IV hypersensitivity?

A
  1. Initiated when tissue macrophages recognise danger signals and initiate an inflammatory response
  2. Dendritic cells loaded with antigen migrate to local lymph node, where present antigen to T cells
  3. Specific T-cell clones proliferate in response to antigens, which migrate to site of inflammation
  4. Tumour necrosis factor (TNF) is secreted by both macrophages and T cells and stimulates much of the damage in delayed hypersensitivities
34
Q

Describe the presentation of rheumatoid arthritis?

A
  • Symptoms arise in joints and tendons, but also affects skin, lungs and eyes
35
Q

Describe the mechanism behind rheumatoid arthritis?

A
  • Antigens that drive RA are citrullinated proteins (citrullination is the conversion of amino acid arginine to the amimo acid citrulline)
  • Autoreactive T and B cells recognise citrullinated proteins, causing production of antibodies against the protein
    • Referred to as anti-cyclic citrullinated peptide (CCP) antibodies
  • Synovium becomes infiltrated by T cells (TH1 and TH17) and macrophages
  • TNF and IL-17 attracts and activates neutrophils that cause damage to synovium
  • Osteoclasts are activated and destroy bone at the joint margins, creating erosions
  • Persistent IL-6 secretion triggers an acute-phase response
36
Q

What are risk factors for rheumatoid arthritis?

A
  • Family history
    • Associated with HLA-DR4
  • Smokers
  • Infection with porphyromonas
37
Q

Describe the mechanism behind MS?

A
  1. Initially, acute attacks occur during which inflammatory lesions consisting of TH1 and TH17 cells and macrophages develop in the affected nervous tissue
  2. Lesions are reversible, relapsing disability typical of early MS
  3. Myelin loss impairs ability of neurons to conduct impulses, resulting in neurological symptoms
  4. Once inflammation settles the disability improves
38
Q

Describe the treatment for delayed hypersensitivity?

A
  • Prevention through avoiding antigens
  • Anti-inflammatory drugs
    • NSAID
    • Corticosteroids
    • Drugs that block TNF and IL-6
    • Antibodies against B cells
  • Immunosuppressive drugs

Immunology and Haematology (23 decks)

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