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IMS - Immunology > Self-recognition, tolerance and hypersensitivity > Flashcards

Self-recognition, tolerance and hypersensitivity Flashcards

1
Q

Define tolerance

A

Immune cells not reacting to antigens

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2
Q

Types of tolerance

A
  • Self tolerance
  • Neonatal tolerance
  • Acquired tolerance
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3
Q

What is self tolerance?

A

Tolerance to innate antigens

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4
Q

What is neonatal tolerance?

A

Tolerance to antigens encountered within hours of being born

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5
Q

What is acquired tolerance?

A

Tolerance to antigens that are encountered throughout life

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6
Q

What is the development of self-tolerance and self-recognition key in?

A

The maturation of T and B cells

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7
Q

What does the breakdown of immunological tolerance lead to?

A

Autoimmune disease

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8
Q

What are immature T cells positively selected for?

A

Recognition of self-MHC molecules

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9
Q

What are immature T cells negatively selected for?

A

Non-recognition of self-peptides

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10
Q

What happens to immature T cells that are not selected in the thymus?

A

Apoptosis

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11
Q

What type of selection do immature B cells undergo in the bone marrow?

A

Negative selection for recognition of self-MHC molecules or other self-antigens

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12
Q

What do T cells have to do in order to correctly function?

A
  • Recognise self-MHC molecules
  • Display self-tolerance
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13
Q

Do B cells show self tolerance?

A

Yes

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14
Q

How do pre T cells in thymus develop self-recognition?

A

Positive selection

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15
Q

How many of the T cells produced will become fully mature immunocompetent cells?

A

1-5%

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16
Q

What happens to self-reactive T cells?

A

Deletion after they leave the thymus should they contact an unrecognised self-protein

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17
Q

What type of tolerance is oral tolerance?

A

Acquired

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18
Q

What is oral tolerance?

A

The acquired ability to not react to antigens in the gut

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19
Q

What occurs when oral tolerance breaks down?

A

Possibly inflammatory bowel disease

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20
Q

What theory explains maternal tolerance?

A

EU-FEDS (eutherian fetoembryonic defense system)

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21
Q

What are the 4 types of hypersensitivity classifications?

A
  • Type 1: IgE mediated (immediate)
  • Type 2: Cytotoxic reaction (complement lysis/ADCC)
  • Type 3: Immune complex reaction (complement activation)
  • Type 4: T-cell mediated (delayed)
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22
Q

What does ADCC stand for?

A

Antibody-dependent cellular cytotoxicity

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23
Q

How long does each type of hypersensitivity classification take to have an effect?

A
  1. 30 minutes
  2. Days
  3. 6-8 hours
  4. 48-72 hours
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24
Q

What is the immune reactant, antigen and effector mechanism of type 1 hypersensitivity?

A
  • Immune reactant: IgE
  • Antigen: soluble antigen
  • Effector mechanism: mast-cell activation
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25
Q

What is the immune reactant, antigen and effector mechanism of type 2 hypersensitivity?

A
  • Immune reactant: IgG
  • Antigen: cell or matrix associated antigen/cell surface receptor
  • Effector mechanism: Complement FcR+ cells (phagocytes, NK cells)/antibody alters signalling
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26
Q

What is the immune reactant, antigen and effector mechanism of type 3 hypersensitivity?

A
  • Immune reactant: IgG
  • Antigen: soluble antigen
  • Effector mechanism: complement phagocytes
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27
Q

What is the immune reactant, antigen and effector mechanism of type 4 hypersensitivity?

A
  • Immune reactant: T1 helper cells/T2 helper cells/CTL
  • Antigen: soluble antigen/Cell associated antigen
  • Effector mechanism: macrophage activation/IgE production, eosinophil activation, mastocytosis/cytotoxicity
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28
Q

Examples of type 1 hypersensitivity reactions

A
  • Allergic rhinitis
  • Allergic asthma
  • Atopic eczema
  • Systemic anaphylaxis
  • Drug allergies
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29
Q

Examples of type 2 hypersensitivity reactions

A
  • Antigen mediated: drug allergies (e.g. penicillin)
  • Cell surface receptor: chronic urticaria (antibody against FcεRI alpha chain)
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30
Q

Examples of type 3 hypersensitivity reactions

A
  • Serum sickness
  • Arthus reaction
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31
Q

Examples of type 4 hypersensitivity reactions

A
  • Helper T1:
    • Allergic contact dermatitis
    • Tuberculin reaction
  • Helper T2:
    • Chronic asthma
    • Chronic allergic rhinitis
  • CTL:
    • Graft rejection
    • Allergic contact dermatitis to poison ivy
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32
Q

What does CTL stand for?

A

Cytotoxic T lymphocyte

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33
Q

General properties of allergens

A
  • Small 15,000-40,000 (molecular weight) proteins
  • Soluble
  • Long-lasting in the environment
  • Low dose of allergen required
  • Mucosal exposure
  • Often proteases
  • Most allergens promote T2 helper cells
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34
Q

Organ manifestation of type 1 reactions

A
  • 45% - skin/mucosa
  • 25% - respiratory tract
  • 20% - gastointestinal
  • 10% - cardiovascular system
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35
Q

Label the protease-mediated type 1 hypersensitivity reaction from a to d

A
  1. Der p 1 cleaves occludin in tight junctions and enters mucosa.
  2. Dendritic cell primes cell in lymph node.
  3. Plasma cell travels back to mucosa and produces Der p 1 specific IgE antibodies.
  4. Der p 1 specific IgE binds to mast cell; Der p 1 triggers mast cell degranulation.
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36
Q

What does Der p stand for?

A

Dermatophagoides pteronyssinus

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37
Q

What are the allergens of Der p 1-14?

A
  1. Cysteine protease
  2. Unknown
  3. Trypsin (serine protease)
  4. Amylase
  5. Unknown
  6. Chymotrypsin (serine protease)
  7. Unknown
  8. Glutathione transferase
  9. Collagenase (serine protease)
  10. Tropomyosin
  11. Apolipophorin like protein
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38
Q

What has proteinase allergens?

A
  • Fungi
  • Insects
  • Plants
  • Parasites
  • Drugs
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39
Q

Are most allergens proteases?

A

No

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40
Q

Label the mast cell activation diagram from a to b

A

a - IgE secreted by plasma cells binds to a high-affinity Fc receptor (FcεRI) on mast cells.

b - Activated mast cells provide contact and secreted signals to B cells to stimulate IgE production.

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41
Q

What are the images on the left and right?

A
  • Left: resting mast cell
  • Right: activated mast cell
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42
Q

Examples of mast cell enzymes

A
  • Tryptase
  • Chymase
  • Cathepsin G
  • Carboxypeptidase
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43
Q

Examples of mast cell toxic mediators

A
  • Histamine
  • Heparin
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44
Q

Examples of mast cell cytokines

A
  • IL-4, IL-13
  • IL-3, IL-5, GM-CSF (Granulocyte-macrophage colony-stimulating factor)
  • TNF-α (Tumor necrosis factor alpha)
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45
Q

An example of a mast cell chemokine

A

CCL3 (Chemokine ligand 3)

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46
Q

Examples of mast cell lipid mediators

A
  • Prostaglandins D2 and E2, leukotrienes C4/D4/E4
  • Platelet activating factor
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47
Q

Biological effects of mast cell enzymes

A

Remodelling of connective tissue matrix

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48
Q

Biological effects of mast cell toxic mediators

A
  • Toxic to parasites
  • Increases vascular permeability
  • Causes smooth muscle contraction
  • Anticoagulation
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49
Q

Biological effects of mast cell cytokines

A
  • IL-4, IL-13
    • Stimulates and amplifies helper T2 cell response
  • IL-3, IL-5, GM-CSF
    • Promotes eosinophil production and activation
  • TNF-α
    • Promotes inflammation
    • Stimulates cytokine production by many cell types
    • Activates endothelium
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50
Q

Biological effects of mast cell chemokine

A

Attracts monocytes, macrophages and neutrophils

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51
Q

Biological effects of mast cell lipid mediators

A
  • Prostaglandins D2 and E2, leukotrienes C4/D4/E4
    • Smooth muscle contraction
    • Chemotaxis of eosinophils, basophils and helper T2 cells
    • Increase vascular permeability
    • Stimulate mucus secretion
    • Bronchoconstriction
  • Platelet-activating factor
    • Attracts leukocytes
    • Amplifies production of lipid mediators
    • Activates neutrophils, eosinophils and platelets
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52
Q

What does mast-cell activation and granule release result in in the gastrointestinal tract?

A
  • Increased fluid secretion and increased peristalsis resulting in:
    • Expulsion of gastrointestinal tract contents
    • Diarrhea
    • Vomiting
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53
Q

What does mast-cell activation and granule release result in in the eyes, nasal passages and airways?

A
  • Decreased diameter and increased mucus secretion resulting in:
    • Congestion and blockage
    • Wheezing
    • Coughing
    • Phlegm
    • Swelling and mucus secretion in nasal passages
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54
Q

What does mast-cell activation and granule release result in in the blood vessels?

A
  • Increased blood flow and permeability resulting in:
    • Increased fluid in tissues
    • Increased flow of lymph to lymph nodes
    • Increased cells and protein in tissues
    • Increased effector response to tissues
    • Hypotension leading to potential anaphylactic shock
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55
Q

What are the common systemic anaphylactic allergens?

A
  • Drugs
  • Venoms
  • Food
  • Serum
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56
Q

What are the routes of entry for systemic anaphylactic allergens?

A
  • Intravenously
  • Orally
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57
Q

What responses to systemic anaphylaxis are there?

A
  • Oedema
  • Increased vascular permeability
  • Laryngeal oedema
  • Circulatory failure
  • Death
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58
Q

What is another term for acute urticaria?

A

Wheel-and-flare

59
Q

What are common allergens of acute urticaria?

A
  • Animal hair
  • Insect bites
  • Allergy testing
60
Q

What are the routes of entry for acute urticaria allergens?

A
  • Through the skin
  • Systemic
61
Q

What is the response to acute urticaria?

A
  • Local increase in blood flow
  • Local increase in vascular permeability
  • Oedema
62
Q

What is seasonal rhinoconjunctivitis commonly known as?

A

Hay fever

63
Q

What are the common allergens of seasonal rhinoconjunctivitis?

A
  • Pollens
    • Ragweed
    • Grass
    • Trees
  • Dust-mite faeces
64
Q

What is the route of entry for allergens of seasonal rhinoconjunctivitis?

A
  • Contact with conjunctiva of eye
  • Nasal mucosa
65
Q

What is the response to seasonal conjunctivitis?

A
  • Oedema of conjunctiva and nasal mucosa
  • Sneezing
66
Q

What are the common allergens of asthma?

A
  • Danders (cat)
  • Pollen
  • Dust mite faeces
67
Q

What is the route of entry for asthma causing allergens?

A

Inhalation leading to contact with lower respiratory system mucous membrane

68
Q

Response to asthma?

A
  • Bronchial constriction
  • Increased mucous production
  • Airway inflammation
69
Q

What are the common food allergens?

A
  • Nuts
  • Fish
  • Dairy
  • Eggs
  • Soy
  • Milk
70
Q

What is the route of entry for food allergens?

A

Orally

71
Q

What is the response to a food allergy?

A
  • Vomiting
  • Diarrhea
  • Pruritis (itching)
  • Urticaria (hives)
  • Anaphylaxis (rare)
72
Q

What are the IgE-mediated allergic reaction?

A
  • Systemic anaphylaxis
  • Acute urticaria
  • Seasonal rhinoconjunctivitis
  • Asthma
  • Food allergies
73
Q

What are symptoms of an IgE-mediated allergic reaction to the upper airways and what is it called?

A
  • Rhinitis
    • Nasal itch
    • Sneezing
    • Rhinorrhea
    • Nasal obstruction
74
Q

What are symptoms of an IgE-mediated allergic reaction to the lower airways and what is it called?

A
  • Asthma
    • Bronchoconstriction
    • Mucous hypersecretion
    • Wheezing
    • Breathlessness
    • Cough
75
Q

What does this image show?

A

Airway inflammation with lymphocytes and eosinophils

76
Q

What does this image show?

A

Airway remodelling with increased collagen deposited around the airway

77
Q

What does the airway inflammation with lymphocytes and eosinophils lead to?

A

Airway remodeling hypertrophy

78
Q

What does airway remodelling with increased collagen deposited around the airway lead to?

A

Fibrosis

79
Q

What are the symptoms of anaphylaxis?

A
  • Extreme hypotension
  • Airway constriction
  • Swelling of the epiglottis
80
Q

What is used to treat an anaphylactic allergic reaction?

A

Epinephrine as it relaxes bronchiole smooth muscles

81
Q

Individuals with what gene mutation experience cold-induced urticaria?

A

NLP3 mutants

82
Q

Which enzyme is involved in the truncation of the inhibitory region PLCG2?

A

Phospholipase

83
Q

Over activation of what gene leads to vibrational urticaria?

A

GPCR-EMR2

84
Q

In individuals with over activation of GPCR-EMR2, what causes mast cell degranulation?

A

Overly sensitive mechanotransduction

85
Q

What are eosinophils?

A
  • Granulocyte that mainly kills opsonised parasites
  • Degranulated by large amounts of IL-5 and IL-3
  • Involved in airway remodelling
86
Q

What are the enzymes of eosinophils?

A
  • Eosinophil peroxidase
  • Eosinophil collagenase
  • Matrix metalloproteinase-9
87
Q

What are the toxic proteins of eosinophils?

A
  • Major basic protein
  • Eosinophil cationic protein
  • Eosinophil-derived neurotoxin
88
Q

What are the cytokines of eosinophils?

A
  • IL-3, IL-5, GM-CSF
  • TGF-α, TGF-β
89
Q

What is the chemokine of eosinophils?

A

CXCL8 (IL-8)

90
Q

What are the lipid mediators of eosinophils?

A
  • Leukotrienes C4, D4, E4
  • Platelet-activating factor
91
Q

What are the biological effects of eosinophil peroxidase?

A
  • Toxic to targets by catalysing halogenation
  • Triggers histamine release from mast cells
92
Q

What are the biological effects of eosinophil collagenase?

A

Remodels connective tissue matrix

93
Q

What are the biological effects of matrix metalloproteinase-9?

A

Matrix protein degradation

94
Q

What are the biological effects of major basic protein?

A
  • Toxic to parasites and mammalian cells
  • Triggers histamine release from mast cells
95
Q

What are the biological effects of eosinophil cationic protein?

A
  • Toxic to parasites
  • Neurotoxin
96
Q

What are the biological effects of eosinophil-derived neurotoxin?

A

Neurotoxin

97
Q

What are the biological effects of IL-3, IL-5 and GM-CSF?

A
  • Amplification of eosinophil production by bone marrow
  • Eosinophil activation
98
Q

What are the biological effects of TGF-α and TGF-β?

A
  • Epithelial proliferation
  • Myofibroblast formation
99
Q

What are the biological effects of CXCL8 (IL-8)?

A

Promotion of influx of leucocytes

100
Q

What are the biological effects of leukotrienes C4, D4 and E4?

A
  • Smooth muscle contraction
  • Increased vascular permeability
  • Increased mucous secretion
  • Bronchoconstriction
101
Q

What are the biological effects of platelet-activating factor?

A
  • Attraction of leucocytes
  • Amplification of lipid mediator production
  • Activation of neutrophils, eosinophils and platelets
102
Q

Why are is allergen sensitivity going up?

A
  • Hygeine hypothesis
  • Rise in Th1/inflammatory immune defects
  • Counter regulation hypothesis
103
Q

What are the clinically used target step treatments for type 1 allergic diseases?

A
  • Mediator action
  • Chronic inflammatory reactions
  • T2 helper cell response
  • IgE binding to mast cell
104
Q

What is the mechanism of treatment for mediator action in type 1 allergic disease?

A
  • Inhibit mediator effects on specific receptors
  • Inhibit specific mediator synthesis
104
Q

What is the mechanism of treatment for chronic inflammatory reactions in type 1 allergic disease?

A

General anti-inflammatory effects

105
Q

What is the mechanism of treatment for T2 helper cells in type 1 allergic disease?

A

Induction of regulatory T cells

106
Q

What is the mechanism of treatment for IgE binding to mast cells in type 1 allergic disease?

A

Bind to IgE Fc region and prevent IgE binding to Fc receptors on mast cells

107
Q

What are the specific approaches for mediator action treatments in type 1 allergic disease?

A
  • Antihistamines, β-blockers
  • Lipoxygenase inhibitors
108
Q

What is the specific approach for chronic inflammatory reaction treatments in type 1 allergic disease?

A

Corticosteroids

109
Q

What is the specific approach for T2 helper cell response treatments in type 1 allergic disease?

A

Desensitisation therapy by injections of specific antigen

110
Q

What is the specific approach for IgE binding to mast cell treatments in type 1 allergic disease?

A

Anti-IgE antibodies (omalizumab)

111
Q

What are the proposed and under investigation target step treatments for type 1 allergic diseases?

A
  • T2 helper cell activation
  • Activation of B cell to produce IgE
  • Mast cell activation
  • Eosinophil-dependent inflammation
112
Q

What is the mechanism of treatment for T2 helper cell activation in type 1 allergic disease?

A

Induction of regulatory T cells

113
Q

What is the mechanism of treatment for activation of B cells, to produce IgE, in type 1 allergic disease?

A
  • Block co-stimulation
  • Inhibit T2 helper cell cytokines
114
Q

What is the mechanism of treatment for mast cell activation in type 1 allergic disease?

A

Inhibit effects of IgE binding to mast cell

115
Q

What is the mechanism of treatment for eosinophil-dependent inflammation in type 1 allergic disease?

A

Block cytokine receptors that mediate eosinophil recruitment and activation

116
Q

What are the specific approaches for T2 helper cell activation treatments in type 1 allergic disease?

A
  • Injection of specific antigens
  • Administration of specific cytokines
  • Use of adjuvants to stimulate a T1 helper cell response
117
Q

What are the specific approaches for activation of B cells, to produce IgE, treatments in type 1 allergic disease?

A
  • Inhibit CD40L
  • Inhibit IL-4 or IL-13
118
Q

What is the specific approach for mast cell activation treatments in type 1 allergic disease?

A

Blockade of IgE receptor

119
Q

What are the specific approaches for eosinophil-dependent inflammation treatments in type 1 allergic disease?

A
  • Inhibit IL-5
  • Block CCR3
120
Q

Did IgE responses evolve to cause allergy?

A

No

121
Q

What did IgE responses evolve to do?

A

Expel and/or destroy helminth and protozoal pathogens

122
Q

What is atopic dermatitis?

A
  • Chronic inflammation, initiated by IgE, causing apoptosis of keratinocytes.
  • Leaky skin allergens cause a filaggrin defect that results in keratin fibres being bound together in the skin.
123
Q

What is the antibody that mediates type 1 allergic disease?

A

IgE

124
Q

What antibody mediates type 2 allergic disease?

A

IgG

125
Q

What allergic diseases are type 2?

A
  • Haemolytic anaemia
  • Thrombocytopenia (haemolytic anaemia in infants)
126
Q

What is haemolytic anaemia?

A

The destruction of blood cells and platelets mediated by IgG antibodies

127
Q

How to IgG antibodies mediate type 2 allergic diseases?

A
  1. Antibodies attach to self epitopes
  2. Induce inflammation compliment activation
  3. Vasodilation and migration of phagocytes to effected tissue
  4. Activation of membrane attack complex
128
Q

What does type 2 allergic antibodies refer to?

A

Antibodies that target self-tissues

129
Q

What are type 3 allergic diseases characterised by?

A

IgG mmune complex formation causing an inflammatory immune response

130
Q

What are some type 3 allergic diseases?

A
  • Arthus reaction
  • Serum sickness
  • Arthritis
  • Vasculitis
  • Nephritis
  • Farmer’s lung
131
Q

Which complement protein sensitises mast cells to respond to IgG immune complexes?

A

C5

132
Q

What does local inflammation in type 3 allergic reaction cause?

A

Occlusion of blood vessels due to the build-up of proteins in the immune response

133
Q

What complex causes a type 3 allergic reaction?

A

Antigen-antibody (IgG) complex

134
Q

What are the two types of type three allergic reaction?

A
  • Local type 3 hypersensitivity
  • Systemic type 3 hypersensitivity
135
Q

What is a local type 3 allergic reaction?

A

Local subcutaneous antigens induce an immune response causing localised inflammation that peaks after approximately 7 hours.

136
Q

What is extrinsic allergic alveolitis caused by and what type of allergic reaction is it?

A
  • Inhaled spores
  • Local type 3 allergic reaction
137
Q

What is a systemic type 3 allergic reaction?

A

Systemic antigen complex formation causing systemic inflammation

138
Q

What causes post-infectious glomerulonephritis and what type of allergic reaction is it?

A
  • Antibody complexes become stuck in the glomeruli of the kidney inducing an inflammatory response.
  • Systemic type 3 allergic reaction
139
Q

What is post-infectious glomerulonephritis most commonly caused by?

A

Streptococcal pharyngitis infections

140
Q

What is another term for type 4 hypersensitivity?

A

Delayed hypersensitivity

141
Q

What mediated type 4 hypersensitivity?

A
  • T1 helper cells
  • Cytotoxic T cells
142
Q

In what time frame does a type 4 allergic reaction happen?

A

24-72 hours after contact with antigen

143
Q

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A

IMS - Immunology (6 decks)

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