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immunology > allergy and hypersensitivity > Flashcards

allergy and hypersensitivity Flashcards

1
Q

What is Type I hypersensitivity?

A

An immediate allergic reaction to environmental antigens, mediated by IgE.

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2
Q

What is atopy?

A

An inherited trait for Type I hypersensitivity.

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3
Q

What are allergens?

A

Antigens that trigger allergic reactions.

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4
Q

What is the first step in Type I hypersensitivity?

A

The body is exposed to allergens, which are taken up by antigen-presenting cells (APCs).

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5
Q

What happens after allergens are presented to T cells?

A

Naive T cells polarise to the Th2 phenotype, producing IL-4 and IL-13.

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6
Q

What role do IL-4 and IL-13 play in sensitisation?

A

They activate B cells, inducing a class switch to IgE production.

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7
Q

Where does IgE bind after being produced?

A

IgE binds to high-affinity receptors on mast cells and basophils.

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8
Q

What is the basic structure of immunoglobulins?

A

Two light chains and two heavy chains linked by disulphide bonds, with variable and constant regions.

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9
Q

What defines the class and function of an antibody?

A

The structure of its heavy chain.

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10
Q

How is IgE different from other immunoglobulins?

A

It has four constant regions and lacks a hinge, making it more flexible and heavily glycosylated.

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11
Q

How is IgE’s half-life prolonged?

A

It is extended to 9-12 weeks when bound to high-affinity receptors on mast cells and basophils

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12
Q

Does IgE activate complement or play a role in bacterial defence?

A

No, it does not activate complement or aid in opsonisation.

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13
Q

What is class switch recombination?

A

A process where B cells rearrange constant region genes to switch from one immunoglobulin type (e.g., IgM) to another (e.g., IgE).

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14
Q

Does class switch recombination change antigen specificity?

A

No, it produces antibodies with different effector properties while retaining the same antigen specificity.

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15
Q

What triggers class switch recombination to IgE?

A

Cytokines like IL-4 promote the switch by activating specific transcription and splicing mechanisms in B cells.

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16
Q

What is the role of T cells in class switch recombination?

A

T cells interact with B cells through CD40 and release cytokines like IL-4 to facilitate the switch.

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17
Q

What triggers mast cell degranulation?

A

Cross-linking of FcεRI receptors on mast cells by the same antigen upon re-exposure.

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18
Q

What happens during mast cell degranulation?

A

The mast cell releases granules containing histamine and other mediators, and new cytokines are synthesised.

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19
Q

What are the two main types of IgE receptors?

A

FcεRI (high-affinity) and FcεRII (low-affinity).

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20
Q

Where is the high-affinity receptor FcεRI found?

A

On mast cells, basophils, smooth muscle cells, dendritic cells, and Langerhans cells.

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21
Q

What is the function of FcεRI?

A

It mediates strong binding of IgE and activates cells via ITAM (Immunoreceptor Tyrosine-based Activation Motif).

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22
Q

What is FcεRII, and where is it found?

A

A low-affinity receptor (CD23) found on B cells, T cells, dendritic cells, eosinophils, platelets, and smooth muscle cells.

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23
Q

What role does ITAM play in IgE receptor signalling?

A

ITAM in β and γ chains of FcεRI mediates intracellular signalling and cell activation.

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24
Q

What activates the high-affinity IgE receptor (FcεRI)?

A

FcεRI aggregation triggers tyrosine kinase activation.

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25
Q

What happens after tyrosine kinase activation in mast cells?

A

Phospholipase C (PLC) is recruited, hydrolysing PIP₂ into DAG and IP₃.

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26
Q

What are the roles of DAG and IP₃ in mast cell activation?

A

DAG: Activates protein kinase C (PKC).
IP₃: Releases calcium from the endoplasmic reticulum.

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27
Q

What is the function of increased calcium and PKC in mast cells?

A

They facilitate microtubule assembly and granule fusion with the plasma membrane for degranulation.

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28
Q

How does FcεRI aggregation promote arachidonic acid synthesis?

A

It converts phosphatidylserine to phosphatidylcholine, which activates phospholipase A2, producing arachidonic acid.

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29
Q

What does arachidonic acid produce, and what is its role?

A

It generates prostaglandins (PGs) and leukotrienes (LTs), which mediate inflammation.

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30
Q

What is the role of MAP kinase in mast cell activation?

A

MAP kinase activates transcription factors, increasing cytokine production.

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31
Q

What is the outcome of mast cell degranulation?

A

Exocytosis of granule-laden vesicles and release of their contents.

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32
Q

What additional process occurs after mast cell degranulation?

A

De-novo production of new cytokines.

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33
Q

What is the ultrastructure of a resting human mast cell?

A

It has a monolobed nucleus, narrow surface folds, and numerous electron-dense cytoplasmic granules.

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34
Q

What is observed in a partially degranulated mast cell?

A

Fewer cytoplasmic granules compared to a resting mast cell, indicating granule release.

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35
Q

What is the original magnification used to observe the mast cell ultrastructure?

A

×15,000.

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36
Q

What are some early-phase mediators released by mast cells?

A

Histamine, tryptase, chymotrypsin, carboxypeptidase A, leukotrienes, prostaglandins, interleukins, PAF, and TNFα.

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37
Q

What does histamine do during an allergic reaction?

A

Causes vasodilation, increases capillary permeability, stimulates nerve endings, and induces bronchoconstriction.

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38
Q

What are the clinical effects of early-phase mediator release?

A

Swelling, redness, itching, wheezing, and other allergy symptoms.

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39
Q

What are the pre-formed mediators released by mast cells?

A
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40
Q

What are the newly synthesised mediators from the lipoxygenase pathway?

A

Leukotrienes C₄, D₄, B₄: Cause bronchoconstriction, vasodilation, and chemotaxis.

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41
Q

What are the newly synthesised mediators from the cyclooxygenase pathway?

A

Prostaglandins and thromboxanes: Affect bronchial muscles, platelet aggregation, and vasodilation.

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42
Q

How is histamine synthesised?

A

By the decarboxylation of histidine.

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43
Q

What happens to histamine after it is released?

A

It is rapidly inactivated.

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44
Q

What are the four subtypes of histamine receptors?

A

H1, H2, H3, and H4.

45
Q

What is the role of H1 receptors in allergic disease?

A

They are responsible for many symptoms of allergic reactions.

46
Q

What additional effects does histamine have?

A

It promotes pro-inflammatory cytokine secretion and chemotaxis of inflammatory cells.

47
Q

What is tryptase, and where is it found?

A

Tryptase is a protease abundant in mast cell granules, stored in a fully processed and active form.

48
Q

What are the variants of tryptase?

A

Alpha, beta, gamma, and delta, with beta-tryptase being the most abundant.

49
Q

When is beta-tryptase detectable in serum?

A

It is usually only detectable after an anaphylactic reaction.

50
Q

What are the functions of tryptase?

A

Increases vascular permeability, recruits cells, and contributes to airway hyperresponsiveness.

51
Q

How does tryptase activity change after an anaphylactic reaction?

A

Levels peak within 30 minutes to 1.5 hours and then taper off gradually.

52
Q

What mediators are released during an allergic reaction?

A

Histamine, tryptase, chymotrypsin, leukotrienes, prostaglandins, and interleukins.

53
Q

What determines the clinical manifestation of an allergy?

A

The site of allergen exposure (e.g., nasal exposure causes rhinitis, ocular exposure causes conjunctivitis).

54
Q

What are some common symptoms of an allergic reaction?

A
55
Q

What is the late-phase response in an allergic reaction?

A

It is a prolonged inflammatory response occurring hours after the immediate reaction, characterised by recruitment of eosinophils and neutrophils.

56
Q

Which cells and mediators contribute to the late-phase response?

A

Cytokines released by T cells and mast cells drive the recruitment of inflammatory cells, such as eosinophils and neutrophils.

57
Q

How does the late-phase response affect symptoms?

A

It can cause a second peak in symptoms hours after the initial reaction, prolonging inflammation and discomfort.

58
Q

When does the late-phase response typically occur?

A

It begins 6–12 hours after the immediate allergic reaction.

59
Q

What conditions elicit a Type I hypersensitivity reaction?

A

Allergen characteristics
Host factors
Environmental influences

60
Q

What are the three key factors in the “triangle” of a Type I hypersensitivity reaction?

A

Host, environment, and allergen.

61
Q

What makes certain proteins allergenic?

A
  • Ability to induce a strong IgE response.
  • Protease activity (e.g., Der p 1).
  • Surface features of the protein (e.g., Ves v 5).
  • Glycosylation pattern of the protein (e.g., Ara h 1).
62
Q

What structural features of proteins contribute to allergenicity?

A
  • Presence of alpha-beta motifs in the tertiary structure.
  • High proportion of hydrophobic residues (indicative of damage).
  • Specific glycosylation patterns important for APC recognition.
63
Q

Why might certain glycosylation patterns in proteins enhance allergenicity?

A

They may resemble glycans displayed by helminths, enhancing recognition by antigen-presenting cells (APCs).

64
Q

What is the role of MHC II in allergy development?

A

It is responsible for antigen recognition (e.g., HLADRB1, HLADQB1).

65
Q

What is the role of TCR in allergic responses?

A

It is responsible for T cell responses to antigen presentation.

66
Q

What does GATA-3 regulate in allergies?

A

Differentiation into the Th2 phenotype and production of cytokines for B cell activation.

67
Q

Which cytokines are involved in allergic responses?

A

IL-4, IL-13, IL-6, IL-10, IL-33, TSLP.

68
Q

What does TNF-α do in allergic reactions?

A

It acts as a pro-inflammatory cytokine.

69
Q

How does FcεRI contribute to allergies?

A

It amplifies the response to activation and stabilises permanence on the membrane.

70
Q

Is allergy a purely genetic disease?

A

No, it is a genetically complex disease influenced by interactions between genes and the environment.

71
Q

What is the Th1/Th2 imbalance in atopic individuals?

A

Atopic individuals have a Th2-dominant response, while early-life infections can shift this towards a Th1 bias.

72
Q

What is the hygiene hypothesis?

A

It proposes that reduced exposure to microbes in industrialised countries increases the incidence of allergies due to diminished immune education.

73
Q

What supports the hygiene hypothesis?

A

Factors like younger siblings, living on a farm, and having pets are associated with reduced allergy incidence.

74
Q

What does the immune regulation theory add to the hygiene hypothesis?

A

It suggests that microbe infections boost regulatory T cells, suppressing both Th1 and Th2 responses to maintain immune balance.

75
Q

How can gut flora and soil microbes influence the immune system?

A

Altered colonisation due to antibiotics or exposure to soil microbes educates the innate immune system on major danger signals.

76
Q

What does the hygiene hypothesis suggest?

A

It suggests that exposure to diverse microbes (e.g., from rural or farm environments) promotes immune tolerance, reducing the risk of asthma and allergies.

77
Q

How does a “westernised” microbiota affect immune balance?

A

A less diverse microbiota increases inflammation, tipping the immune balance towards asthma and allergies.

78
Q

What environmental factors promote immune tolerance?

A

Exposure to archaic microbiota (e.g., helminths).
Living in rural or farm environments.

79
Q

What triggers inflammation in a “westernised” setting?

A
  • Pollution and environmental exposure.
  • Viral infections (e.g., sinusitis).
  • A poor diet affecting microbiota diversity.
80
Q

What types of allergens might early mammal ancestors have been exposed to?

A
  • Pollen from early plants (cycads, ferns, conifers).
  • Fungal spores.
  • Exo- and ectoparasites (e.g., ticks, fleas, lice, mosquitoes).
  • Allergens in food (insects, nuts, seeds).
  • Venomous animals (scorpions, spiders).
81
Q

What was the role of allergic responses in early mammals?

A

Allergic responses may have acted as gatekeepers at mucosal surfaces, expelling noxious substances through sneezing, vomiting, diarrhoea, or coughing.

82
Q

How is IgE involved in allergic and anti-parasitic responses?

A

IgE mediates Th2 responses, helping eosinophils kill parasites and expel allergens.

83
Q

What additional role do platelets play in allergic responses?

A

Platelets assist eosinophils in killing parasites via IgE and FcεRI.

84
Q

What are pseudo-type I reactions?

A

Non-IgE-mediated mast cell degranulation caused by various factors.

85
Q

What factors can trigger pseudo-type I reactions?

A
  • Drugs (e.g., opiates, NSAIDs, IV contrast media, ACE inhibitors).
  • Physical stress.
  • Psychological stress.
  • Concurrent infection.
  • Autoimmune disease.
  • Nutritional status (e.g., deficiencies in iron, vitamin B12, vitamin D).
86
Q

What are the primary treatments for anaphylaxis?

A
  • Adrenaline/Epinephrine (vasoconstriction via alpha-adrenergic stimulation).
  • Antihistamines (block histamine H1 receptors).
  • Corticosteroids (reduce pro-inflammatory protein transcription).
  • Fluid resuscitation.
  • Bronchodilation.
87
Q

How does adrenaline work in anaphylaxis?

A

It counters vasodilation and vascular permeability, reducing hypotension and stabilising circulation.

88
Q

What is Omalizumab?

A

A recombinant DNA-derived humanised monoclonal antibody that binds to IgE and prevents it from binding to the high-affinity IgE receptor (FcεRI).

89
Q

What are the treatment applications of Omalizumab?

A

Licensed for asthma and urticaria.
Used in cases of severe allergic conditions where other treatments are insufficient.

90
Q

What is the role of leukotriene antagonists in treatment?

A

They are used in asthma to reduce airway inflammation and bronchoconstriction.

91
Q

What is desensitisation or allergen-specific immunotherapy?

A

A process where the immune system is exposed to gradually increasing doses of an allergen to develop tolerance.

92
Q

How is allergen-specific immunotherapy administered?

A

Via subcutaneous or sublingual routes.

93
Q

What conditions is allergen-specific immunotherapy commonly used for?

A

Allergic rhinitis, venom allergy, and drug allergies.

94
Q

What are the key considerations for desensitisation therapy?

A
  • Typically takes around 3 years.
  • Risk of anaphylaxis exists.
  • Peanut allergy desensitisation is also available.
95
Q

How is asthma classified in terms of hypersensitivity mechanisms?

A

Asthma involves type I hypersensitivity, type IV (cell-mediated), and type V (tissue-driven) mechanisms.

96
Q

What is a common characteristic of a large proportion of asthmatics?

A

They have T2-high (T2-hi) inflammation.

97
Q

What modern treatment options are available for asthma?

A

Numerous monoclonal antibodies targeting specific pathways and cells involved in asthma.

98
Q

Name some monoclonal antibodies used in asthma treatment.

A

Dupilumab
Omalizumab
Benralizumab
Mepolizumab
Reslizumab
Tezepelumab
Itepekimab

99
Q

What enzyme does aspirin inhibit, and what is its role?

A

Aspirin inhibits COX-1, which is primarily responsible for the prostaglandin arm of the pathway, involved in histamine release inhibition, bronchodilation, and vasodilation.

100
Q

What happens when aspirin inhibits COX-1 in sensitive individuals?

A

It shunts arachidonic acid to the lipoxygenase (5-LO) pathway, increasing leukotrienes like LTC₄, LTD₄, and LTE₄, causing bronchoconstriction, vasoconstriction, and increased vascular permeability.

101
Q

What are the effects of leukotrienes produced in aspirin sensitivity?

A

Bronchoconstriction
Vasoconstriction
Mucus hypersecretion
Increased vascular permeability
Eosinophil and neutrophil chemotaxis

102
Q

Why are NSAID-intolerant asthmatics more COX-1 dependent?

A

Due to low COX-2 activity, they rely on COX-1 for PGE₂ production, which helps prevent excessive leukotriene synthesis.

103
Q

What are key symptoms in aspirin/NSAID sensitivity reactions?

A

Increased bronchoconstriction, mucus hypersecretion, and inflammation mediated by leukotrienes.

104
Q

What is the role of angiotensin-converting enzyme (ACE)?

A

ACE catalyzes the conversion of angiotensin I to angiotensin II (a potent vasoconstrictor) and degrades bradykinin (a potent vasodilator).

105
Q

What happens when ACE inhibitors block ACE activity?

A

Bradykinin accumulates, leading to vasodilation, increased vascular permeability, and potentially bronchoconstriction.

106
Q

What are the effects of angiotensin II in the body?

A

Vasoconstriction, vascular hypertrophy, and aldosterone release.

107
Q

How common are adverse reactions to ACE inhibitors due to bradykinin accumulation?

A

They occur in less than 1% of patients on ACE inhibitors.

108
Q

What additional factors may contribute to adverse reactions to ACE inhibitors?

A

Defects in bradykinin degradation pathways.

immunology (8 decks)

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