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SEM 4: Immunology > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

1
Q

What are the four types of hypersensitivity?

A
  1. Immediate hypersensitivity
  2. Cytotoxic hypersensitivity
  3. Serum sickness and arthus reaction
  4. Delayed-type hypersensitivity, contact dermatitis
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2
Q

Describe what happens during an immediate hypersensitivity reaction

A
  1. Results from being exposed to allergens in the environment e.g. house dust mites
  2. The host generates an immune response characterised by IgE antibodies.
  3. The IgE antibodies are attached to immune cells called mast cells.
  4. When exposed to the allergen to which the IgE is specific, the IgE is crosslinked and activates the inflammatory cells to release mediators causing inflammation.
  5. The inflammatory mediators cause local oedema in the tissues = wheel, vasodilatation and a flare response.
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3
Q

Which allergens is the immediate hypersensitivity reaction common in?

A

Common in allergic rhinitis (pollen, hay fever), asthma and anaphylaxis (vasodilatation and oedema - need adrenaline).

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4
Q

How long does it take the immediate hypersensitivity reaction take in?

A

Response within 10-15 mins

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5
Q

How can an immediate hypersensitivity reaction be induced?

A

It can be induced by injecting an allergen into the skin or even by scratching the surface. This is how they do allergy testing as the mast cells will crosslink and cause the release of inflammatory mediators.

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6
Q

What causes a cytotoxic reaction?

A

It is caused by an immune response generated against altered components of human cells. For example, people allergic to penicillin can modify proteins on human cells and an immune response will be generated.

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7
Q

Describe what happens during the cytotoxic hypersensitivity reaction

A
  1. The immune response recognises a drug (for example) on a cell and sees it as foreign.
  2. It generates an IgG immune response.
  3. The cell coated by IgG activates cells containing the IgG receptor. This activates macrophages and complement leading to inflammation.
    This response is associated with drug allergies such as penicillin.
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8
Q

What is a special case of a type II response?

A

It involves IgG antibodies directed at cell-surface receptors. These antibodies disrupt the normal functions of the receptor by either; uncontrollable activation or blocking receptor function e.g. myasthenia gravis or Graves’ disease

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9
Q

What happens during Graves’ disease and the cytotoxic hypersensitivity reaction?

A
  1. Normally, the pituitary gland releases TSH which causes the thyroid to release thyroxine.
  2. This has a negative feedback mechanism to decrease the amount of TSH released.
  3. In an autoimmune response, a response is generated against the receptor, leading to excess levels of TSH in the blood with no negative feedback.
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10
Q

What happens during myasthenia gravis and the cytotoxic hypersensitivity reaction?

A
  1. Normally, a neuromuscular junction is activated and releases acetylcholine which stimulates receptors on the muscle cell causing contraction.
  2. However, sometimes there is an immune response against receptors on the postsynaptic junction which blocks the nerve transmission resulting in paralysis.
  3. The antibodies can block or destroy the nAchR at the junction between the nerve and the muscle.
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11
Q

Describe the haemolytic disease of the newborn

A
  • Blood group antigen group on RBC called rhesus (Rhd).
  • A Rhd -ve mother can have a Rhd +ve child and develop an immune response against the rhesus antigen.
  • This will happen at the time of delivery and the embryonic chorion normally isolates the fetal and maternal blood.
  • But what happens, there is disruption of the embryonic chorion resulting in release of RBC in the maternal circulation and the body creates an immune response against the antigen, in the first pregnancy.
  • In a second pregnancy, the antibodies can cross the placenta and attack the RBC causing anaemia and death in the child.
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12
Q

Describe what happens during the serum sickness/Arthus reaction

A
  1. There is a presence of a soluble antigen e.g. vaccine to which there is an IgG response already generated.
  2. Large amounts of antigen and antibody at the site of infection can cause the formation of immune complexes in the tissues.
  3. These can activate the cells around the capillaries such as mast cells. This will cause the release of inflammatory mediators.
  4. The inflammatory cells invade the site, and blood permeability and blood flow increases.
  5. Platelets also accumulate, leading to occlusion of the small blood vessels, haemorrhage and the appearance of purpura.
  6. This causes an inflammatory response and activation of complement, causing more inflammation.
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13
Q

What does the Arthus reaction or serum sickness response depend on?

A

The type of response is dependent on the antigen dose and the route of delivery.

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14
Q

What is the response when antigen dose is injected intravenously?

A

It can cause inflammation in the blood vessels casuing vasculitis, nephritis (caused by inflammation in the renal glomeruli) and arthritis (inflammation in the joint spaces).

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15
Q

What is the response when antigen dose is injected subcutaneously?

A

It causes a localised arthus reaction with a localised perivascular area.

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16
Q

What is the response when the antigen is inhaled?

A

It can cause farmer’s lung where there is inflammation at the alveolar-lung interspace.

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17
Q

Describe the arthus reaction following the diphtheria/tetanus vaccination

A

Elevated levels of antibodies and when vaccinated again can cause an immune complex disease resulting in localised inflammation

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18
Q

What can cause serum sickness?

A

Caused when large amounts of antigen injected intravenously into circulation e.g. drugs or horse immunoglobulin used to treat snake bites.

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19
Q

What gives farmer’s farmer’s lung?

A

When farmer’s are exposed to hay with mould. These are inhaled and cause localised inflammation in the lung. The antigen inhaled forms an immune complex in the alveoli which causes an immune response. This can result in fibrosis, granulation and inflammation.

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20
Q

What mould causes farmer’s lung?

A

thermophilic actinomycosis

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21
Q

What is pigeon breeder’s lung?

A

Another form of farmer’s lung, where people are exposed to pigeon proteins which causes a response called interstitial pneumonitis.

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22
Q

What is Bagazosis? And what causes Bagazosis?

A

Bagazosis is caused by people exposed to sugar cane production. There is mould in the sugar cane during the processing so they can inhale it. This can cuase localised inflammation in the lungs and a type III hypersensitivity reaction.

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23
Q

What is delayed-type hypersensitivity reaction?

A

The classical form is related to the type of immune cells released i.e. Th1 (helper cell associated with immune response to things like intracellular bacteria) or Th2 (helper cell associated with immune response to allergens or worm infections).

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24
Q

Describe the Th1 delayed-type hypersensitivity reaction

A
  1. An antigen, such as tuberculin, stimulates Th1 cells to produce interferon-gamma and IL-12.
  2. This forms a cognate interaction with specific T cells that recognise the antigen.
  3. These stimulate classical macrophages to release chemokines and cytokines.
  4. These recruit cells to the site of inflammation, in this case, forming a tuberculin granuloma. It takes about 2-3 days to form.
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25
Q

How many days should you wait to see if you are sensitive to tuberculin?

A

If doing a test, wait 2-3 days to see if you are sensitive to tuberculin.

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26
Q

What is the Mantoux Test?

A

Injection of an extract of tuberculin and wait to see if there is a reaction to it. This shows if someone has been sensitised to tuberculin already.

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27
Q

What is the Th2 delayed-type hypersensitivity reaction?

A
  1. When exposed to allergen or worm infections, the Th2 cells produce cytokines such as IL-4 and IL-5.
  2. These are important in Ig production and recruitment of eosinophils to the site of infection.
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28
Q

When does a Th2 delayed-type hypersensitivity reaction occur?

A

This is seen in allergic contact dermatitis (e.g. nickel).

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29
Q

What causes a strong contact dermatitis type reaction in poison ivy?

A

Pentadecacatechol

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30
Q

Define an allergy

A

A disease following a response by the immune system to an otherwise innocuous antigen e.g. house dust mites

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31
Q

What are the forms of IgE-mediated allergic reactions?

A
  • Systemic anaphylaxis
  • Acute urticaria (wheal-and-flare)
  • Allergic rhinitis
  • Asthma
  • Food allergy
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32
Q

What causes systemic anaphylaxis?

A

Exposure to drugs/serum/venon/peanuts for exampel and causes a profound systemic response with activation of mast cells and systemic oedema

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33
Q

When does acute urticaria occur?

A

Occurs in response to things such as animal hair, insect bites and allergy testing by a localised skin reaction.

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34
Q

What causes allerfic rhinitis?

A

Involves breathing in things through the nose and get a reaction in the nasal mucosa causing irritation.

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35
Q

What causes asthma?

A

After exposure to pollens, hair etc by inhalation can cause bronchoconstriction. Increased mucus production and airway inflammation.
Highest prevalence is in the USA and the western world.

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36
Q

What can a food allergen cause?

A

It can cause vomiting, diarrhoea etc after oral exposure.

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37
Q

What is IgE?

A

An immunoglobulin molecule. It is different in terms of structure compared to IgG - has one extra domain in the heavy chain.

  • Coats inflammatory cells such as mast cells and basophils that have a high affinity receptor as well as eosinophils.
  • Developed evolutionarily to combat worm infections.
38
Q

Describe allergen-specific IgE production

A
  1. First exposure to pollen causes activation of the immune response.
  2. APC picks up the pollen and takes them to lymph nodes where they activate immune cells such as Th2 cells.
  3. Th2 releases IL-4 that activates B-cells that have the same specificity for allergens to produce IgE.
  4. IgE is released in circulation and binds to mast cells waiting for the next exposure to the allergen.
39
Q

What causes allergic sensitisation?

A
  • Exposure to allergen is crucial
  • Role of pro-allergic dendritic cells and cytokines: certain types of APC are more likely to produce a Th2 response depending on the local environment and tissues.
  • Genetic predisposition to allergy
40
Q

What does the exposure to the allergen include?

A
  • The nature of the allergen: usually a protein but also can be carbohydrates
  • Dosage of allergen (high is associated with tolerisation)
  • Timing: early or later in life
  • Location of priming e.g. airways or skin etc
41
Q

What are some common allergens?

A

House dust mites
Pollen
Cockroaches
Not all allergens are proteins; some received in small doses and a higher dose exposure may lead to tolerance.

42
Q

How are allergens classified?

A

Classified systematically based on the source of the organism and the order they were discovered.

43
Q

What is the genetics of allergy?

A

There is no single gene that explains allergy. A number of genes explain a small variation. But the interaction between genes and the environments is also very important.

44
Q

What is the function of filaggrin?

A
  • Important in maintaining the skin integrity.
  • People who lack this gene are far more likely to have a less effective skin barrier.
  • This means that things are more likely to enter so greater access for allergens.
45
Q

Why is the type of cell that presents the allergen important?

A

It is important in determining whether there is an allergic or non-allergic response.

46
Q

Which cells in the skin are important in presenting allergens to the immune response?

A

In the normal skin, there is epidermis, APCs called langerhans and dendritic cells.

47
Q

What happens when the epidermis or epithelium is injured?

A

This can induce cells such as keratinocytes which are pro-Th2 and a molecule such as TSLP to produce an immune response.

48
Q

How is an immune response generated in response to allergies?

A
  1. Exposure to an antigen e.g. pollen
  2. The immune response is primed for a Th2 response. The Th2 and B-cells recognise the same antigen and there is a cognate interaction between the cells.
  3. This stimulates the Th2 cell to produce IL-4 which causes the B-cell to produce IgE.
  4. The IgE lines the mast cells and subsequent exposure causes activation of the mast cell causing hayfever.
49
Q

What happens when mast cells are activated?

A

A resting mast cell is full of dense granules which contain inflammatory mediators such as histamine.
An activated mast cell releases the granules and has a completely different structure.

50
Q

What are the two phases in the allergic response?

A

Early and Late phase response

51
Q

What is the early response in an allergic reaction?

A

When exposed to an allergen, there is an activation of mast cells which releases the mediators and causes the early response e.g. wheal-and-flare response.

52
Q

What is the late response in an allergic reaction?

A

When the allergen dose is high, it can cause a late response, the level of activation will cause recruitment of other immune cells to the site of reaction which causes a later immune response that is associated with T cells.

53
Q

What is FEV1?

A

The amount of air that is blown out as quickly as possible in one second. This gives an idea of lung function.

54
Q

What happens to the FEV1 when exposed to an inhaled allergen?

A

There is a reduction in the FEV1 due to bronchoconstriction almost 30 mins following inhalation.

55
Q

What happens to the FEV1 in the second response to the allergen?

A

It returns to normal, however after recruitment of more cells in the late response, there is a second response to the allergen, this is longer and lasts about 6-8 hours or even up to 24 hours.

56
Q

Symptoms of early response: acute allergic reaction

A
  • Wheezing
  • Urticaria
  • Sneezing, rhinorrhea
  • Conjunctivitis
57
Q

Symptoms of late response: chronic allergic reaction

A
  • Further wheezing
  • Sustained blockage of the nose
  • Eczema
58
Q

What are the effector mediators released in the early phase?

A
  • Release of histamine
  • Release of leukotrienes
  • Release of prostaglandins
59
Q

What does histamine do?

A

increases vascular permeability and causes smooth muscle contraction

60
Q

What do leukotrienes do?

A

increases vascular permeability, causes smooth muslce contraction and stimulates mucus secretion

61
Q

What do prostaglandins do?

A

chemoattractants for T cells, eosinophils and basophils

62
Q

What are the effector mediators released in the late phase?

A
  • release cytokines such as IL-4 and IL-13 that promote Th2 and IgE
  • release cytokines such as TNF-alpha to promote tissue inflammation
63
Q

What is the effect of mast cells on the GI tract?

A

The mast cells will release mediators that will increase fluid secretion and peristalsis to get rid of the worms as this will lead to explusion of GT contents.

64
Q

What is the effect of mast cells on the airways?

A

This causes airways to constrict which increases mucus production resulting in blockage of the airways and wheezing.

65
Q

What is the effect of mast cells on the blood vessels?

A

It causes increased blood flow and increased permeability which increases fluid in tissues causing increased lymph flow. The classic wheal-and-flare response.

66
Q

What is the function and location of eosinophils?

A
  • Located in the tissues
  • Recruited to the sites of allergic reactions
  • Express FceRI (high affinity Ig receptor) upon activation.
67
Q

What are the two effector functions of eosinophils?

A
  1. Release highly toxic granule proteins and free radicals upon activation to kill microorganisms/parasites but also cause tissue damage as the eosinophils release toxic mediators.
  2. Synthesise and release prostaglandins, leukotrienes and cytokines which amplify the inflammatory response.
68
Q

What is the late phase of the IgE-mediated allergic response?

A

The late-phase reaction is dependent on allergen dose.

  1. There is continued synthesis and release of inflammatory mediators.
  2. The chronic allergic inflammation caused by Th2 cells i.e. a type IV hypersensitivity reaction.
  3. It is T-cell mediated: mostly Th2 cells and these cells recruit other cells by cytokine release that potentiate further responses.
  4. This forms a chronic inflammatory response.
69
Q

What is the difference between sensitisation to allergen and reaction to an allergen?

A

A individual must be sensitised to an allergen before they can react.

70
Q

What happens when a person is sensitisation to a allergen?

A

It requires presentation of allergen to T cells by DC and the priming of cognate B cells to produce IgE. (A cognate B cell recognises the same antigens as the T cells).

71
Q

What is a reaction to an allergen defined as?

A

It occurs when the individual is re-exposed to allergen and it binds pre-formed IgE on mast cells.

72
Q

Define asthma

A

A state of reversible bronchial hyper-reactivity resulting from a persistant inflammatory process in response to a number of stimulin in a genetically suspectible individual.

73
Q

What is the name for allergic and non-allergic asthma?

A 
Allergic = atopic asthma 
Non-allergic = non-allergic asthma
74
Q

What are the different forms of non-atopic asthma?

A

Occupational
Exercise induced
Nocturnal asthma
Children have post-bronchiolitis wheeze

75
Q

What are the characteristics of atopic asthma?

A
  • Wheezy breathing episodes
  • Narrowing of the airways
  • Rapid changes in airway obstruction
  • Severity varies: slight wheeziness to asthma attack
76
Q

Which common allergens can cause asthma?

A

Pollen
HDM
Plants
Some food

77
Q

What is the acute response that happens in allergic asthma?

A

It occurs within seconds and results in airway obstruction and difficulty breathing. This caused by allergen-induced mast cell degranulation in the submucosa of the airways.

78
Q

What is the chronic response that happens in allergic asthma?

A

This is a T-cell mediated response. There is inflammation of the airways caused by activation of eosinophils, neutrophils, T cells (Th2) and other leukocytes. Mediators released by these cells cause airway remodelling, permanent narrowing of the airway, and further tissue damage.

79
Q

What happens in chronic asthma?

A

Lose the reversal of the airways; more overlap with COPD

80
Q

What do normal airways look like?

A
  • Smooth muscle
  • Epithelial layer
  • Mucus in the epithelium
  • Open lumen to allow breathing
81
Q

What do (acute) obstructured asthma airways look like?

A
  • Contracted smooth muscle
  • Oedema of the submucosa
  • Increased mucus production
  • Reduces diameter of the lumen
  • Restricted airflow and wheezing
82
Q

What do (chronic) damaged airways look like?

A
  • Bronchus can completely obstructed by mucus

- Inflammatory damage with remodelling of the airway such as fibrosis and further damaged

83
Q

What needs to happen to treat asthma?

A

Remove the blockage to the airway and stop the production of mucus

84
Q

What do antihistamines do?

A

Inhibit effects of mediators on specific receptors by blocking histamine H1 receptor

85
Q

What do mast cell stabilisers do?

A

Chromoglycate for example which inhibit mast cell degranulation so no release of inflammatory mediators that recruit cells to the site of inflammation

86
Q

What do lipoxygenase inhibitors do?

A

Motelukast for example; inhibit synthesis of specific mediators such as leukotrienes and cytokines

87
Q

What is most commonly used to treat asthma?

A

Steroids and bronchodilators

88
Q

Give an example of a steroid used and how they work

A

Prednisolone - Steroids are inhaled and act on DNA to increase transcription of anti-inflammatory mediators such as IL-10 and decrease transcription of pro-inflammatory mediators

89
Q

What do bronchodilators do and give an example?

A

Reverse the acute effect of allergy on airways. An example is beta 2 agonists such as salbutamol.

90
Q

What type of therapy can be used to treat asthma?

A

Use immunotherapy as it can reverse the sensitisation to allergen by means of tolerising exposure

SEM 4: Immunology (15 decks)

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