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POM 4 Immunology > 4.8 Hypersensitivity > Flashcards

4.8 Hypersensitivity Flashcards

1
Q

What is meant by hypersensitivity?

A

Immune reaction that damages the body rather than protecting it from infection

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2
Q

What is the name of type I hypersensitivity?

A

Immediate/anaphylactic hypersensitivity

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3
Q

What are type I hypersensitivity reactions mediated by?

A

IgE antibodies

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4
Q

What is type I hypersensitivity triggered by?

A

Multivalent environmental antigens (allergens)

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5
Q

What 2 phases does type I hypersensitivity occur in?

A

Sensitisation

Re-exposure leading to anaphylaxis

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6
Q

Which 3 factors influence the initial sensitisation of the immune response to allergens?

A

Genetics, age, environment

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7
Q

Outline the sensitisation phase of type I hypersensitivity

A

APC present antigen and co-stimulatory molecule to T cell

Naive T cell becomes primed and differentiates into TH2 cell

TH2 cells release IL4 and 12 to promote class switching from IgM to IgE, and IL5 which activates eosinophils

IgE then bind FcE receptors on mast cells

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8
Q

Outline what happens in second exposure in type I hypersensitivity

A

Allergen binds to IgE on mast cells, crosslinking two IgE molecules

This causes rapid degranulation, releasing pro inflammatory mediators (histamines, cytokines, leukotrienes, prostaglandins)

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9
Q

What effects does histamine have?

A

Binds to H1 receptors

Causes bronchoconstriction, vasoconstriction, increased vascular permeability

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10
Q

What effects do leukotrienes have?

A

Smooth muscle contraction

Recruit neutro/eosinophils/mast cells after allergen is cleared

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11
Q

What happens if an allergen encounters cell bound IgE?

A

Rapid cross linking of IgE and degranulation of the mast cell

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12
Q

What happens in the early phase of type I hypersensitivity?

A

Effects of molecules released in mast cell degranulation

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13
Q

When does the early phase of type I hypersensitivity occur?

A

Few minutes after second exposure

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14
Q

What happens in the later phase of type I hypersensitivity?

A

Recruitment of neutrophils

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15
Q

When does the later phase of type I hypersensitivity occur?

A

Within a few hours

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16
Q

What happens in the late phase of type I hypersensitivity and when?

A

Eosinophils are recruited and TH2 cells are present

3-4 days after exposure

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17
Q

Which of an anaphylactic shock reaction or immune complex reaction requires more antigen to trigger?

A

Immune complex requires more antigen

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18
Q

List 3 treatments for type I hypersensitivity

A

Antihistamines – reduce bronchoconstriction and vascular permeability

Corticosteroids – decrease inflammatory response

Adrenaline – cause vasoconstriction

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19
Q

What causes anaphylactic shock?

A

Decrease in blood supply to vital organs (e.g. the brain) due to increased vascular permeability and increased airway constriction

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20
Q

What is the name of type II hypersensitivity?

A

Antibody mediated cytotoxic hypersensitivity

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21
Q

What does type II hypersensitivity involve?

A

The destruction of cells/tissue by IgG or IgM antibodies that bind to antigens present on the surface of normally healthy cells

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22
Q

What are examples of type II hypersensitivity reactions?

A
  1. Graves disease – antibodies bind to thyrotrophin receptor resulting in the over production of thyroid hormones
  2. Haemolytic disease of newborn – maternal antibodies can cross the placenta and destroy fetal red blood cells
  3. Immune thrombocytopenia – antibodies develop against platelets
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23
Q

What are the three mechanisms by which type II hypersensitivity reactions can occur?

A
  1. Anti-receptor activity
  2. Antibody dependant cell mediated cytotoxicity
  3. Classical activation of the complement cascade
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24
Q

Outline the first mechanism of complement activation in type II hypersensitivity

A

IgM/IgG binds an antigen that is bound to the surface of a healthy cell and activates complement

C1 binds Fc region of antibody and recruits other complement proteins

The proteins that are cleaved are chemotactic – attract neutrophils

Neutrophils degranulate and release enzymes that produce ROS, causing cell death

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25
Q

What enzymes do neutrophils release when they degranulate?

A

Myeloperoxidase, peroxidase, proteinase 3

26
Q

Outline the second mechanism of complement activation in type II hypersensitivity

A

Complement proteins form membrane attack complexes

MACs create holes in the cell membrane, causing cell death by water influx

27
Q

Outline the third mechanism of complement activation in type II hypersensitivity

A

C3b binds IgG antibodies coating a cell

Cell becomes opsonised and targeted for phagocytosis

Antibody-antigen complex and cell encounters phagocytes in the spleen

Phagocyte binds Fc tail or C3b, engulfing the cell

28
Q

Outline antibody dependent cell-mediated cytotoxicity as a cytotoxic mechanism of type II hypersensitivity

A

NK cells recognise the antigen-antibody complex, specifically the Fc tail

Thus they release granules that contain perforin

Perforin forms pores in the cell membrane which allow granzymes and granulysin to enter and trigger apoptosis

Inflammatory mediators, chemokines and cytokines are also released

29
Q

Outline antibody-mediated cellular dysfunction

A

Antibody stops antigen from binding receptor

30
Q

How does antibody-mediated cellular dysfunction work in myasthenia gravis?

A

Antibody blocks Ach receptors, thus muscles weaken over time

31
Q

How does antibody-mediated cellular dysfunction work in graves disease?

A

Antibody targets and binds TSH receptors on thyroid follicular cells, causing overproduction of thyroid hormone

32
Q

How does type 2 hypersensitivity cause tissue damage?

A

Local or systemic inflammation

Cell depletion thus loss of function

Imbalance in organ function

33
Q

How do you test for autoimmune haemolytic anemia?

A

Direct coomb’s test

Antibodies are separated from plasma and mixed with coomb’s reagent which is anti-human globulin (antibodies against human antibodies)

If agglutination occurs, this indicates presence of antibody

34
Q

What happens in type III hypersensitivity?

A

When immune complexes cannot be cleared and are thus deposited in blood vessel walls and tissue, causing inflammation and tissue damage

35
Q

What is an immune complex?

A

Soluble antigens bound to antibody

(i.e. non-cell bound antigen-antibody complexes)

36
Q

Why do immune complexes deposit in blood vessel basement membranes?

A

The small complexes are less immunogenic, thus less attracted to macrophages and less easily removed

37
Q

What is the difference between complement activation in type 2 and type 3 hypersensitivty?

A

Type III uses complement proteins in large amounts compared to type II

38
Q

What issues can type III hypersensitivity lead to?

A

Fever, rash, protein in blood, joint pain

Glomerulonephritis – kidney
Arthritis – joints
Vasculitis – blood vessel walls

39
Q

What effect do C3 and C4 have in type III hypersensitivity?

A

They act as chemokines by attracting neutrophils to the side

40
Q

What do neutrophils do when they arrive at the immune complexes in type III hypersensitivity?

A

They degranulate and result in tissue necrosis and vasculitis

41
Q

What happens in systemic lupus erythmatosus?

A

IgG is produced against DNA self-antigens released from damaged cells

Thus IgG-DNA autoantigen complexes form and remain in blood vessels, depositing on the basement membrane

When deposited, they activate the complement system

42
Q

What happens when complement is activated in systemic lupus erythmatosus?

A

Complement proteins act as:

Anaphylatoxins – increase vascular permeability, leading to oedema
Chemokines – recruit neutrophils which degranulate, releasing enzymes that produce ROS, causing vasculitis

43
Q

What types of antigens cause type 3 hypersensitivity?

A

Autoantigens
Foreign antigens (e.g. from persistent infection)

44
Q

Describe serum sickness

A

Patient given serum with anti-venom antibodies

Exposure to foreign antibody in serum triggers B cells to differentiate into plasma cells and produce IgG against the foreign antibody

If the serum is given a second time, IgG forms immune complexes with the anti-venom antibodies, causing vasculitis and tissue necrosis

45
Q

What is a membrane attack complex?

A

Fragments of the complement system form a complex which attaches to the cell surface membrane

This creates a channel that disturbs the osmotic integrity of the cell, causing lysis

46
Q

Why do immune complexes not initiate complement cascade?

A

Classical complement pathway involves formation of MAC which occurs in cell walls, whilst immune complexes are free floating

47
Q

What are the primary cells involved in type IV hypersensitivity reactions?

A

T cells

48
Q

What causes type IV hypersensitivity?

A

CD8 T cells releasing cytotoxic granules
CD4 T cells releasing cytokines
APCs presenting antigens

49
Q

Outline the sensitisation phase in type IV hypersensitivity

A

Dendritic cells carry antigen to draining lymph node

CD4+ T cells recognise antigen and bind MHCII with TCR and CD4 receptor

Dendritic cell releases interleukins, causing differentiation into Th1 cells

Th1 cells release IL-2 for the proliferation of other T cells and IFN-gamma for macrophage activation

50
Q

What do activated macrophages do in type IV hypersensitivity?

A

Release pro-inflammatory cytokines, causing leaky endothelial barriers and immune cell recruitment

Release lysosomal enzymes, complement proteins and ROS, causing tissue damage

51
Q

What’s the most common example of type IV hypersensitivity and what happens?

A

Contact dermatitis due to poison ivy

Small molecules urushiol acts as hapten and binds proteins in skin

Upon re-exposure, memory T cells release cytokines that promote pro-inflammatory activation of macrophages, causing oedema, swelling and lesions

52
Q

What do active macrophages release?

A

Pro-inflammatory cytokines like TNF, IL-1 and IL-6

53
Q

Which Interleukin has an autocrine effect?

A

IL-2

54
Q

The test for what infection is conducted via the means of a type 4 hypersensitivity reaction?

A

Tuberculin skin test, where a protein from mycobacterium tuberculosis is injected into the skin

In a positive test – TB-specific TH1 cells migrate to site of injection, cause induration (skin becomes thick and hard)

55
Q

Why are type IV hypersensitivity reactions called the delayed type?

A

It takes 48-72 hours to recruit TH1 cells to the site

56
Q

In which auto-immune disease do patients develop IgGs against DNA or proteins present in the nucleus, forming persistent immune complex deposits and a variety of pathologies?

A

Systemic lupus erythematosus

57
Q

What symptoms can immune complexes not being efficiently cleared lead to?

A

Symptoms such as fever, rashes, joint pain or protein in the urine

58
Q

What needs to occur before T cells can initiate type IV?

A

Sensitisation phase where antigen is presented to naive T cells by antigen presenting dendritic cells

Results in the generation of antigen specific memory T cells

59
Q

What systemic diseases are type IV hypersensitivity involved in?

A

Multiple sclerosis – Th1 cells damage myelin around nerve fibres

Inflammatory bowel disease – Th1 cells cause inflammation in intestinal lining

60
Q

Give an example where TH2 cells cause type IV hypersensitivity

A

Asthma, where allergens cause Th2 overreaction

This produces soluble mediators, leading to bronchoconstriction

61
Q

What other antigens can cause type IV hypersensitivity?

A

Nickel salts, hair dyes, intracellular pathogens

62
Q

Give 3 examples where CD8+ T cells cause type IV hypersensitivity

A

Type 1 diabetes mellitus – attacks pancreatic islet cells
Hashimoto’s thyroiditis – attacks thyroid epithelial cells
Graft rejection – destruction of transplanted cells

POM 4 Immunology (14 decks)

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