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Immunology > Session 1: Hypersensitivity Reactions > Flashcards

Session 1: Hypersensitivity Reactions Flashcards

1
Q

What is the most common cause of immunodeficiency in the UK?

A

Malnutrition age >65 yo

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2
Q

Define hypersensitivity.

A

The antigen-specific immune responses that are either inappropriate or excessive and result in harm to host.

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3
Q

What three questions do you have to ask yourself when presented with a hypersensitivity reaction?

A

Trigger of reaction

Mechanism of reaction

Target tissue/organ of reaction

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4
Q

Give broad types of triggers (antigens).

A

Exogenous antigens

Intrinsic antigens

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5
Q

Give categories of exogenous antigens.

A

Non infectious substances

Infectious microbes (e.g. sepsis)

Drugs like penicillin

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6
Q

Give common non-infectious substances triggering a reaction.

A

Pollen

Dust

Cats/dogs

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7
Q

Give categories of intrinsic antigens.

A

Infectious microbes (mimicry)

Self-antigens (auto-immunity)

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8
Q

Explain infectious microbes and mimicry.

A

An example is rheumatic fever where the microbe has a simlar structure to an internal antigen and triggers a reaction.

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9
Q

Types of hypersensitivity reactions.

A

Type I

Type II

Type III

Type IV

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10
Q

What is type I also called?

A

Immediate allergic reactions where there is a reaction to an environmental non-infectious antigen.

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11
Q

What is type II also called?

A

Antibody mediated.

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12
Q

What is type III also called?

A

Immune complexes mediated reaction

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13
Q

What is type IV also called?

A

Cell mediated (delayed) by environmental infectious agents and self antigens.

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14
Q

What is the difference between Type I-III and Type IV?

A

Type I-III are antibody mediated.

Type IV is cell mediated.

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15
Q

Phases of hypersensitivity.

A

Sensitisation phase

Effector phase

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16
Q

Explain sensitisation phase.

A

First encounter with the antigen where there is activation of APCs and memory effector cells.

A previously exposed individual to the antigen is said to be “sensitised”.

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17
Q

Explain effector phase.

A

Pathologic reaction upon re-exposure to the same antigen and activation of the memory cells of the adaptive immunity.

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18
Q

How fast does type II hypersensitivity usually develop?

A

Within 5-12 hours

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19
Q

What antibodies do type II hypersensitivity involve?

A

IgG

IgM

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20
Q

What do the antibodies (Most commonly IgG) target?

A

Cell bound antigens.

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21
Q

Give example of cell bound antigens targeted by IgG in type II HS.

A

Exogenous such as blood group antigens and Rhesus D antigens.

Endogenous such as self antigens.

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22
Q

Types of outcomes of type II HS.

A

Tissue/cell damage

Physiological change of

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23
Q

Give examples of type II HS mechanisms of tissue/cell damage.

A

Via complement activation where there is cell lysis via MAC.

Neutrophil recruitment and activation via C3a and C5a

Opsonisation via C3b and C4b

Antibody-dependent cell cytotoxicity via NK cells.

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24
Q

Give examples of disease due to tissue/cell damage in type II hypersensitivity.

A

Haemolytic disease of the newborn (HDN) due to antigen Rhesus D.

Transfusion reactions where the antigen is ABO system.

Autoimmune haemolytic anaemia

Immune thrombocytopenia purpura

Anti-GBM

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25
Q

Give an example of disease caused by type II HS with IgM involvement.

A

Haemolytic transfusion reaction

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26
Q

Complications of haemolytic transfusion reaction.

A

Shock

Kidney failure

Circulatory collapse

Death

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27
Q

Explain the immune mechanism in haemolytic transfusion reaction.

A

There is an incompatibility in the ABO or Rhesus D antigens.

The donor RBC is destroyed by the recipient’s immune system.

RBC lysis induced by type II hypersensitivity involving by the naturally occurring antibodies IgM.

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28
Q

Give an example of disease caused by type II hypersensitivity with IgG.

A

Haemolytic disease of the newborn.

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29
Q

Explain the immune mechanism in HDN.

A

An Rh+ father shags an Rh- mother.

Father knocks up Rh- mother, shame.

The foetus is Rh+. This is not usually a problem as the bloods don’t mix. However during delivery there is almost always some mixing of blood and some of the Rh+ blood from foetus ends up in the mother.

The mother will develop antibodies against Rh+ (IgG anti-RhD).

The mother is now sensitised and if she has another baby with Rh+ blood the IgG antibodies can diffuse across the placenta and end up in the foetal blood. The antibodies will then attack the red blood cells and induce HDN.

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30
Q

How can HDN be prevented?

A

By giving RhoGAM which is an RhD immune globulin.

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31
Q

Mechanism of RhoGAM.

A

RhD immune globulin which is given to the mother within 72 hours of delivery.

This drugs will bind to RhD and destroy them so the mother won’t be exposed to it in time.

32
Q

Give examples of physiological change in type II HS.

A

Receptor stimulation

Receptor blockade

33
Q

Give an example of receptor stimulation in type II HS.

A

Graves’ disease where there is increased thyroid activity.

34
Q

What is the antigen in graves’ disease?

A

The antigen is the TSH receptor which TSI will bind to.

35
Q

Give an example of a receptor blockade type II hypersensitivity.

A

Myasthenia gravis where there is impaired neuromuscular signalling.

36
Q

What is the antigen in myasthenia gravis?

A

ACh receptor

37
Q

What is given in type II HS of complement activation?

A

Anti-inflammatory drugs

38
Q

What is given in type II HS of circulating antibodies and inflammatory mediators?

A

Plasmapheresis

39
Q

What is can be done if there is a problem where there is too much opsonisation or phagocytosis?

A

Splenectomy can be done.

40
Q

What is given in type II HS of IgG degradation?

A

Intravenous Immunoglobulin IVIG

41
Q

Tx of Graves’.

A

Antithyroid drugs or removal of thyroid

42
Q

Tx of Myasthenia gravis.

A

Pyridostigmine (ACh esterase inhibitor)

Corticosteroids

43
Q

Give conditions where plasmapheresis might be done.

A

Myasthenia gravis

Anti-GBM

Graves’ disease

Plasmapheresis is done because the diseases are antibody driven. Remove the antibody -> remove symptoms

44
Q

Explain plasmapheresis therapy.

A

Blood is filtered and the plasma is separated from the blood. The plasma is then filtered again and the antibodies are filtered out.

The plasma is then reintroduced to the blood alongside with some substitution fluid.

45
Q

Time frame of type III Hs.

A

Usually develops within 3-8 hours

46
Q

What is involved in type III HS?

A

Immune complexes between IgG or IgM and antigens.

47
Q

What is targeted in type III HS?

A

Soluble antigens.

48
Q

What is the importance of soluble antigens being targeted in type III HS and not membrane bound?

A

That it is circulating antigens that are targeted and not membrane bound.

This means that the reactions are usually systemic.

49
Q

Give examples of soluble antigens targeted in Type III HS.

A

Foreign like an infection

Endogenous like self antigens.

50
Q

How is tissue damage caused in type III HS?

A

By deposition of the immune complexes.

51
Q

What are the key factors affecting IC pathogenesis?

(Immune complex)

A

Complex size

Host response

Local tissue factors

52
Q

Why does size matter in IC pathogenesis?

A

Small and large size ICs are usually and easily cleared.

Intermediate size ICs are difficult to get rid of.

53
Q

Why can complement deficiency lead to type III HS?

A

Because the complement system is important in order to clear large size immune complexes.

54
Q

Where might you see persistence of ICs depositions?

A

Joints

Kidneys

Small vessels

Skin

55
Q

Explain the type III HS immune mechanism.

A

Intermediate sized immune complexes are deposited in the tissue.

This leads to activation of complement system. C3a and C5a drives neutrophil chemotaxis and activation. C3b and C4b drives opsonisation.

The neutrophil will adhere to the tissue and cause degranulation and pick up the intermediate immune complex via Fcgamma receptor.

The degranulation that neutrophils cause releases enzymes and reactive oxygen species that will cause tissue damage.

56
Q

Explain mechanism behind RA.

A

A self-antigen where the antigen is the Fc portion of IgG.

There will be articular and extra-articular features where there are episodes of inflammation and remission.

57
Q

What suggests a poor prognosis of RA.

A

<30 y/o when onset.

High-titre of Rheumatoid factor

Female

DR4 allele

Joint erosions.

58
Q

Give another example of disease caused by Type III HS.

A

Glomerulonephritis which is infectious due to bacterial endocarditis or Hep B infection.

59
Q

Antigen in SLE.

A

Ds-DNA.

This is the most prevalent immune complexes disease (Type III)

60
Q

Most commonly affected of SLE (m vs f)

A

Female 9:1 Male

61
Q

Onset of type IV HS.

A

Usually develops within 24-72 hrs.

62
Q

What cells does type IV HS involve?

A

Lymphocytes

Macrophages

63
Q

Give examples of subtypes of type IV HS.

A

Contact HS

Tuberculin HS

Granulomatous HS

64
Q

Explain the pathogenesis of type IV HS.

A

A sensitation phase where the antigen presenting cell will trigger a Th1 response.

There is then an effector phase where the Th1 cell will bind and activate a resting macrophage via IFN-gamma and TNF-beta.

The new activated macrophage will recruit more TNF and cause a granuloma e.g.

65
Q

Explain contact HS.

A

Occurs within 48-72h after exposure.

It is an epidermal reaction which requires an endogenous protein.

66
Q

Examples of common contact HS.

A

Nickel (very common)

Poison ivy

Organic chemicals

67
Q

Explain granulomatous HS.

A

Occurs around 21-48 days after exposure.

It will result in tissue damage and it has to do with when the body can’t get rid of the microbe so it builds a fort around it.

68
Q

Give examples of granulomatous HS.

A

Tuberculosis

Leprosy

Schistosomiasis

Sarcoidosis

69
Q

Explain tuberculin HS.

A

Occurs within 48-72 hours and is a dermal reaction.

70
Q

Give examples of when tuberculin HS might be induced medically.

A

Mantoux test in checking for TB

Lepromin test for leprosy.

71
Q

Give examples of diseases caused by type IV HS to endogenous antigens.

A

Insulin-dependent DM

Hashimoto’s thyroiditis

Rheumatoid arthritis.

72
Q

Explain the pathogenesis of Hashimoto’s.

A

CD4 T cell becomes a helper T cell. Stimulating B cell production and CD8 T cells.

The B cell is autoreactive and becomes a plasma cell.

The plasma cell then causes necrosis and apoptosis of thyroid cell.

The CD8 T cell is autoreactive and become a CTL (cytotoxic T lymphocyte).

CTLs will trigger apoptosis of thyroid cell leading to hypothyroidism.

73
Q

Explain the pathogenesis of Graves’ disease.

A

CD4 T cell becomes T helper cell and then induces B cell activity called TSH-reactive B cell.

The B cell becomes a plasma cell which has TSI.

TSI will bind to its antigen (TSH) leading to hyperthyroidism.

(This is type II)

74
Q

Give examples treatments in type III and type IV HS.

A

Anti-inflammatory drugs

Monoclonal antibodies

75
Q

Give examples of anti-inflammatory drugs.

A

Non-steroidals

Corticosteroids

Steroid sparing such as azathioprine, mycophenolate mofetil, cyclophosphamide.

76
Q

Give examples of monoclonal antibodies.

A

B cells and T cells

Cytokine network

APCs.

Immunology (6 decks)

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