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Immunology Y2 > Hypersensitivity and Allergy > Flashcards

Hypersensitivity and Allergy Flashcards

1
Q

Atopy is…

A

A form of allergy in which there is a hereditary or constitutional tendency to develop hypersensitivity reactions in response to allergens (atopens)- individuals with this predisposition, and conditions provoked in them by contact with allergens, are described as atopic

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2
Q

What does an appropriate immune reaction involve

A
  • Involves antigen recognition by cells of the immune system and antibody production
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3
Q

Antigen recognition + ‘danger’ signals =

A

IMMUNE REACTIVITY

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4
Q

Antigen recognition + no ‘danger’ signals =

A

Tolerance

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5
Q

What leads to tolerance

A

Antigen recognition + no ‘danger’ signals

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6
Q

What leads to IMMUNE REACTIVITY

A

Antigen recognition + ‘danger’ signals

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7
Q

HYPERSENSITIVITY REACTIONS:

 Occur when immune responses are mounted against: (3)

A
  1. Harmless foreign antigens (allergy/contact hypersensitivity)
  2. Autoantigens (autoimmune diseases)
  3. Alloantigens (serum sickness, transfusion reactions, graft rejections)
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8
Q

Immune response against what causes allergy/contact hypersensitivity

A

Harmless foreign antigens

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9
Q

Immune response against what causes serum sickness, transfusion reactions, graft rejections

A

Alloantigens

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10
Q

Alloantigens are against what? (3)

A

serum sickness, transfusion reactions, graft rejections

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11
Q

4 types of hypersensitivity reactions?

A
  • Type I: Immediate Hypersensitivity
  • Type II: Antibody-dependent Cytotoxicity
  • Type III: Immune Complex Mediated – complex of antibody and antigen causing disease
  • Type IV: Delayed Cell Mediated
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12
Q

What is a type 1 hypersensitivity reaction (summarised)

A

Immediate Hypersensitivity

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13
Q

What is a type 2 hypersensitivity reaction (summarised)

A

Antibody-dependent Cytotoxicity

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14
Q

What is a type 3 hypersensitivity reaction (summarised)

A

Immune Complex Mediated – complex of antibody and antigen causing disease

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15
Q

What is a type 4 hypersensitivity reaction (summarised)

A

Delayed Cell Mediated

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16
Q

Examples of type 1 hypersensitivity? (4)

A

Anaphylaxis, asthma, rhinitis (seasonal or perennial (long lasting, year round i.e. constant)), food allergies

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17
Q

Explain 2 exposure mechanism of T1 hypersensitivity

A

1st EXPOSURE:
- Sensitisation (allergy) not tolerance (no allergy)
- Sensitisation involves IgE antibody production
- IgE binds to Mast Cells and Basophils
2nd EXPOSURE:
- More IgE Ab produced
- Antigen cross-links IgE on Mast Cells/Basophils
- Leads to degranulation and release of inflammatory mediators

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18
Q

What Ab does sensitisation involve

A
  • Sensitisation involves IgE antibody production

- IgE binds to Mast Cells and Basophils

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19
Q

What cells do IgE act on in T1 hypersensitivity

A

Mast Cells/Basophils

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20
Q

Examples of diseases caused by T2 hypersensitivity reactions? (4+3)

A
  • Myasthenia gravis (anti-ACh receptor antibodies)
  • Glomerulonephritis (anti-glomerular basement membrane antibody)
  • Pemphigus vulgaris (anti-epithelial cell cement protein antibody)
  • Pernicious anaemia (antibody mediated blood cell destruction such as below)
  • Haemolytic anaemia
  • Thrombocytopenia
  • Neutropenia
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21
Q

What autoimmune target when attacked causes pemphigus vulgarisms

A

autoimmune attack of an antibody that cements epithelial cells together

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22
Q

What autoimmune target when attacked causes bullies pemphigoid

A

antibodies are against basement membrane proteins

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23
Q

Difference between pemphigus vulgarisms and bulls pemphigoid?

A

the blisters tend to be more robust because they are due to a deeper inflammation in the skin than pemphigus

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24
Q

What is used to test for specific antibodies in T2 HS (2)

A
  • Immunofluorescence
  • ELISA (enzyme-linked immunosorbent assay, e.g. anti-CCP cyclic citrullinated peptide antibodies for rheumatoid arthritis)
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25
Q

Examples of diseases caused by T3 hypersensitivity reactions? (3)

A
  • Tissue damage (vasculitis)
    Systemic lupus erythematosus (SLE)
    Vasculitides (Poly Arteritis Nodosum, many different types)
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26
Q

What causes T3 HS?

A
  • Formation of Antigen-Antibody complexes in blood
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27
Q

Explain mechanism of T3 hypersensitivity reactions (4 stages)

A
  • Formation of Antigen-Antibody complexes in blood they can’t get through small blood vessels very easily
  • This causes complex deposition in blood vessels/tissue
  • This leads to complement and cell activation
  • Activation of other cascades e.g. clotting
  • Tissue damage (vasculitis)
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28
Q

Examples of T4 HS reactions? (8)

A
  • Chronic graft rejection
  • GVHD (Graft vs host disease)
  • Coeliac disease
  • Contact hypersensitivity
  • Many autoimmune diseases
  • Asthma (this and below are Th2 mediated, above is Th1 mediated )
  • Rhinitis
  • Eczema
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29
Q

3 main varieties of T4 HS reaction?

A
  1. Th1
  2. Cytotoxic
  3. Th2
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30
Q

What characterises TH1 mediated T4 HS?

A

Characterised by producing lots of gamma-interferon- the most important type in hypersensitivity reactions

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31
Q

What characterises TH2 mediated T4 HS?

A

Releases IL-4, IL-5 and IL-13:

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32
Q

Which IFN is most important in hypersensitivity

A

gamma-interferon

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33
Q

Explain TH2 mediated T4 HS?

A
  • Th2 mediates allergic inflammation e.g. asthma etc.
  • Mechanisms involve either a transient antigen presence or a persistent antigen
  • T cells then activate macrophages and CTLs
  • Much of the tissue damage is dependent upon TNF, hence why neutralising TNF has marked clinical benefits
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34
Q

examples of Th1 mediated diseases in T4 HS? (5)

A
  • Chronic graft rejection
  • GVHD (Graft vs host disease)
  • Coeliac disease
  • Contact hypersensitivity
  • Many autoimmune diseases
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35
Q

examples of Th2 mediated diseases in T4 HS? (3)

A
  • Asthma
  • Rhinitis
  • Eczema
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36
Q

Explain mechanism of T4 mediated HS? (3)

A
  • Transient/Persistent antigen
  • T cell activation of macrophages, CTLs
  • Much of tissue damage dependent upon TNF & CTLs
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37
Q

What is the antigen in T2 HS reactions?

A

Cell surface or matrix bound proteins

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38
Q

What is the antigen in T3 HS reactions?

A

Soluble antigens

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39
Q

What causes asthma? Ig involved, what cell is involved, what is induced, and what does this produce?

A

caused by IgE binding to mast cells and by the induction of T cells producing Th2 type cytokines

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40
Q

4 signs of inflammation?

A
  1. Vasodilation, increased blood flow  leads to redness
  2. Increased vascular permeability Caused by C3a, C5a, histamine and leukotrienes  leads to swelling
  3. Inflammatory mediators and cytokines
  4. Inflammatory cells and tissue damage  leads to pain
41
Q

5 cytokines involved in inflammation? (3 IL, 2 other)

A

IL-1, IL-2, IL-6, TNF, IFN-gamma

42
Q

Chemokine involved in inflammation? (2)

A

IL8/CXCL8, IP-10/CXCL10

43
Q

What mediates cell trafficking?

A

chemokines

44
Q

Which Ig is linked to atopy?

A

IgE

45
Q

Which gene cluster and chromosomes are linked to atopy

A

IL-4 gene cluster (Chr 5)

chromosome 11q

46
Q

Environmental risk factors for atopy? (6)

A
  • Age allergies rare in infancy, peaks in teens, reduces in adulthood
  • Gender Asthma is more common in males in childhood, females in adulthood
  • Family size More common in small families
  • Infections Early life infections protect against atopy
  • Animals Early exposure to animals protects against atopy
  • Diet Breast feeding, anti-oxidants and fatty acids protect against atopy
47
Q

Why is the prevalence of allergies largely increasing? (2)

A

Prevalence of allergies are increasing largely due to change in the environment (less grass n trees n shit) and because infectious diseases are a lot less common now than they were back in the day

48
Q

What types of inflammation is seen in T1 HS? What mediates this?

A

Anaphylaxis, urticarial, angioedema
Asthma, rhinitis, eczema

IgE

49
Q

What types of inflammation is seen in T2 HS? What mediates this?

A

Idiopathic/chronic urticaria  type II hypersensitivity (IgG mediated)
Asthma, rhinitis, eczema

IgG mediated)

50
Q

What types of inflammation is seen in T4 HS? What mediates this?

A

Asthma, rhinitis, eczema

51
Q

What mediates inflammation in T2 HS?

A

IgG

52
Q

Explain how sensitisation occurs in atopic airway disease starting with CD4 T cells being activated

A

CD4+ T cells are activated by an antigen presenting cell, they become specific to the presented antigen

  • They could become Th1 (producing IFN-gamma leading to autoimmune disease)
  • They could become Th2 cells that lead to the activation of B cells which will lead to allergic response

Th2 cells then proliferate and release IL4 and IL13 which stimulates proliferation and differentiation of B cells and causes them to produce IgE instead of IgG which is specific to that peptide of allergen.

If the T cell was presented with a harmless antigen, it may become a regulatory T cell leading to tolerance

53
Q

Explain what happens in the second exposure of T1 HS starting with allergens being presented

A

allergens are presented by the APCs to the memory Th2 cells

  • These release IL-5 which activates and causes degranulation of eosinophils releasing bare mediators of inflammation
  • Th2 cells also release IL-4 and IL-13, which stimulate the production of IgE by plasma cells
  • The IgE then becomes mobilized onto the surface of mast cells
  • The antigens then cross-link with the IgE on the surface of the mast cells and cause degranulation
  • There is a massive release of inflammatory mediators, which gives rise to the effects seen in an allergic reaction
54
Q

What does IL 5 cause

A

activates and causes degranulation of eosinophils releasing bare mediators of inflammation

55
Q

What IL does a Th2 cell release in HS

A

IL-5, IL-4 and IL-13

56
Q

What does IL4 and IL13 do

A

stimulate the production of IgE by plasma cells

57
Q

What 3 lymphocytes are recruited during allergic reactions

A

EOSINOPHILS
MAST CELLS
NEUTROPHILS

58
Q

Number of lobes in the nucleus of an eosinophil?

A

2

59
Q

Eosinophils are mainly found where

A

In tissues

60
Q

Receptors on the surface of mast cells?

A

IgE

61
Q

What do mast cells release on activation via IgE (5)

A

Pre-formed Histamine, cytokines, toxic proteins

Newly synthesized Leukotrienes, prostaglandins

62
Q

What newly synthesised molecules do mast cells release? (2)

A

Leukotrienes, prostaglandins

63
Q

What pre-formed molecules do mast cells release? (3)

A

Histamine, cytokines, toxic proteins

64
Q

Neutrophils cause what types of asthma (3)

A

Virus induced, severe asthma and atopic eczema

65
Q

of Lobes in the nucleus of neutrophils?

A

Polymorphonuclear, so quite a few

66
Q

Granules of neutrophils contain what, and what do neutrophils synthesis (4)

A

digestive enzymes Oxidant radicals
Cytokines
leukotrienes

67
Q

Which HS types are involved in asthma?

A

is a mixture of type 1 and type 4

68
Q

Granules of eosinophils contains what?

A
  • toxic proteins
69
Q

What cell mediates acute airway narrowing in asthma? (cell and what it releases (4))

A
  • Mast cell activation and degranulation releases histamines (pre-stored mediators) and prostaglandins and leukotrienes (newly synthesized mediators)
70
Q

Acute Airway narrowing caused by What 3 processes?

A
  1. Vascular leakage leading to airway wall oedema
  2. Mucus secretion filling up the lumen
  3. Smooth muscle contraction around the bronchi
71
Q

What 4 things occur during chronic inflammation of the airways?

A
  • Smooth muscle hypertrophy
  • Mucus plugging
  • Epithelial shredding
  • Sub-epithelial fibrosis (if the inflammation has persisted for a long time) causing permanent airway narrowing from scarring.
72
Q

What 2 cells infiltrates the airways during inflammation?

A

Th2 lymphocytes and eosinophils

73
Q

9 clinical features of asthma?

A
  • Reversible generalized airway obstruction Causes chronic episodic wheeze
  • Bronchial hyper-responsiveness (they are much more sensitive to bronchial irritants
  • Cough
  • Mucus production
  • Breathlessness
  • Chest tightness
  • Response to treatment
  • Spontaneous variation
  • Reduced and variable peak expiratory flow (PEF)
74
Q

What are the 2 responses in asthma?

A

early response which is immediately after inhalation of the allergen and the late response which is cell mediated

75
Q

How much after inhalation of allergen can the large response occur

A

5 hours give or take

76
Q

what causes the early response to asthma?

A

largely due to mast cell activation

77
Q

what causes the late response to asthma? (2)

A

due to neutrophils and eosinophils.

78
Q

2 types of allergic rhinitis?

A
  • Seasonal- e.g. hay fever (grass and tree pollens)

- Perennial- house dust mites, animal allergens etc.

79
Q

Symptoms of allergic rhinitis? (4)

A
  • Sneezing
  • Rhinorrhoea
  • Itchy nose and eyes
  • Nasal blockage, sinusitis, loss of smell/taste
80
Q

What can eczema lead to?

A
  • Can lead to house dust mite sensitization The dust mite proteins can get through the dry, cracked skin
81
Q

what HS type is food allergy? What mediates. this reaction?

A

Type I (IgE mediated) hypersensitivity reaction

82
Q

Common food allergies?

A

Eggs, cow’s milk in babies n toddlers

Peanuts, shellfish, nuts, fruits, cereals, soya in children n adult

83
Q

Mild symptoms of food allergy?

A
  • Itchy lips and mouth
  • Angioedema
  • Urticaria (hives)
84
Q

Severe symptoms of food allergy? (4)

A
  • Nausea
  • Abdominal pain
  • Diarrhoea
  • Anaphylaxis
85
Q

What mediates anaphylaxis?

A

Generalised degranulation of IgE sensitized mast cells

86
Q

Symptoms of anaphylaxis? (6)

A
  • Itchiness around mouth, pharynx and lips
  • Swelling of lips, throat and other parts of the body
  • Wheeze, chest tightness and dyspnea
  • Faintness, collapse
  • Diarrhea &vomiting (D&V)
  • Death if severe and untreated
87
Q

Effects of anaphylaxis on body systems? (4)

A

CVS Vasodilation, cardiovascular collapse
Respiratory Bronchospasm, laryngeal oedema
Skin Vasodilation, erythema, urticarial, angioedema
GI D&V^

88
Q

Investigation and diagnosis of anaphylaxis? (5)

A
  • Careful history is essential
  • SKIN PRICK TESTING
  • RAST (radioallergosorbent test) Tests for the amount of specific IgE antibodies in the blood
  • Measure total IgE
  • Lung function (in asthma)
89
Q

Emergency treatment for anaphylaxis? (severe and mild)

A
  • EpiPen and anaphylaxis kit (antihistamine steroid and adrenaline)
  • Emergency treatment if mild = antihistamine (can be backed up with a steroid injection)
  • Emergency treatment if severe = ADRENALINE
90
Q

Methods of Prevention of anaphylaxis? (4)

A
  • Avoidance of known allergen
  • Always carry EpiPen and anaphylaxis kit
  • Inform immediate family and caregivers
  • Wear a MedicAlert bracelet
91
Q

Treatment for rhinitis? (2)

A

Anti-histamines

Nasal steroids

92
Q

Treatment for eczema??

A

Emollients for moisture

Topical steroid cream

93
Q

What is salbutamol used for

A

Asthma

94
Q

What is the MoA of salbutamol

A

Short acting b2 agonist

95
Q

4 stems to treat asthma?

A

1 - short acting beta 2 agonist (salbutamol)
2 - inhaled steroid (budesonide)
3 - Add therapy (long acting B2 agonist or leukotriene antagonist
And inhaled high dose steroids
4 - add oral steroids, prednisolone and anti-IgE, Anti-IL4/13 and anti-IL5 mAbs

96
Q

How does immunotherapy work in building tolerance?

A
  • Make people develop tolerance by exposing them to small amount of the allergen they’re allergic to
97
Q

What is immunotherapy effective in building tolerance for?

A

for single antigen hypersensitivities

98
Q

2 types of immunotherapy?

A
  • Subcutaneous immunotherapy (SCIT)

- Sublingual immunotherapy (SLIT)

Immunology Y2 (5 decks)

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