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Year 2 - Immunology > Hypersensitivity and allergy > Flashcards

Hypersensitivity and allergy Flashcards

(49 cards)

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1
Q

What are the appropriate situations in which immune tolerance occurs?

What happens in immune tolerance?

A

Appropriate immune tolerance occurs to self, and to foreign harmless proteins:
- Food, pollens, other plant proteins, animal proteins, commensal bacteria

Involves antigen recognition and generation of:

  • Regulatory T cells
  • Regulatory (blocking) antibody (IgG4) production
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2
Q

What are hypersensitivity reactions?

A

Hypersensitivity Reactions occur when immune responses are mounted against

  • Harmless foreign antigens (allergy, contact hypersensitivity)
  • Auto-antigens (autoimmune disease)
  • Allo-antigens (serum sickness, transfusion reactions, graft rejection)
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3
Q

What is an allloantigen?

A

An antigen present only in some individuals (e.g. of a particular blood group) and capable of inducing the production of an alloantibody in people that lack it

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4
Q

What is the classification of hypersensitivity?

A

Type I: Immediate Hypersensitivity

Type II: Antibody-dependent Cytotoxicity

Type III: Immune Complex Mediated

Type IV: Delayed Cell Mediated

Many diseases involve a mixture of different types of hypersensitivity

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5
Q

Give examples of type 1 hypersensitivity

A
  • Anaphylaxis
  • Asthma
  • Rhinitis: seasonal and perennial
  • Food Allergy
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6
Q

What is the mechanism of type 1 hypersensitivity (immediate hypersensitivity)?

A

1st Antigen exposure:

  • Sensitisation not tolerance
  • IgE antibody production -> IgE binds to mast cells & basophils

2nd Antigen Exposure:

  • More IgE antibody produced -> antigen cross-links IgE on mast cells and basophils
  • This leads to degranulation and release of inflammatory mediators
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7
Q

Give examples of type 2 hypersensitivity

(antibody-dependent)?

A

Organ-specific autoimmune diseases

  • Myasthenia gravis (Anti-acetylcholine R antibodies)
  • Glomerulonephritis (Anti-glomerular basement membrane antibodies)
  • Pemphigus vulgaris (Anti-epithelial cell cement protein antibodies)
  • Pernicious anaemia (Intrinsic factor blocking antibodies)

Autoimmune cytopenias (antibody-mediated blood cell destruction)

  • Haemolytic anaemia
  • Thrombocytopenia
  • Neutropenia
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8
Q

How can we test for specific autoantibodies?

A
  • Immunofluorescence

- ELISA e.g. anti-CCP for rheumatoid arthritis

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9
Q

What is pemphigus vulgaris and bullous pemphigoid?

A

Pemphigus vulgaris: due to autoimmune attack of an antibody that cements epithelial cells together.

Bullous pemphigoid: another blistering skin disorder (antibodies are against BM proteins) so the blisters tend to be a bit more robust because they are due to a deeper inflammation in the skin than pemphigus

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10
Q

What is type 3 hypersensitivity (immune complex mediated hypersensitivity)? Give the mechanism and examples

A
  • Formation of antigen-antibody complexes in blood
  • They can’t get through the small blood vessels easily -> complexes deposit in the vessels and tissues
  • This leads to complement activation and cell recruitment/activation
  • Activation of other cascades e.g. clotting
  • Tissue damage (vasculitis):
    Systemic lupus erythematosus (SLE)
  • Vasculitides (Poly Arteritis Nodosum, many different types)
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11
Q

What are the most common sites of vasculitis?

A

renal (glomerulonephritis), skin, joints and lung

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12
Q

Give examples of type 4 (delayed type hypersensitivity)?

A
  • Chronic graft rejection
  • Graft-versus-host disease (GVHD)
  • Coeliac disease
  • Contact hypersensitivity
  • Many others: asthma, rhinitis, eczema
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13
Q

What do Th1 and Th2 cells do?

A

Th1 - characterised by producing lots of gamma-interferon. Th1 is important in most hypersensitivity reactions. Th2 releases: IL-4, IL-5 and IL-13.

Th2 mediates allergic inflammation e.g. asthma, rhinitis and eczema. 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-alpha; hence why neutralising TNF-alpha has marked clinical benefits

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14
Q

….

A

Hypersensitivity types 1-3 are mediated by antibody and the type of antigen that they recognise distinguishes them.

Type 2 = cell surface or matrix bound antigens

Type 3 = soluble antigens

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15
Q

….

A

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

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16
Q

What is the purpose of inflammation?

A
  • This is the body’s response to tissue injury
  • It is a rapid attempt to bring the body’s defences to the site of injury
  • Immune cells are recruited and they release cytokines which cause the features of inflammation
  • Inflammatory mediators: complement, cytokines
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17
Q

What are the features of inflammation?

A
  • Vasodilatation, increased blood flow
  • Increased vascular permeability
  • Inflammatory mediators & cytokines
  • Inflammatory cells & tissue damage
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18
Q

What happens during inflammation, what causes the features?

A
  • Increased vascular permeability: caused by C3a, C5a, histamine, leukotrienes
  • Cytokine release: IL-1, IL-6, IL-2, TNF, IFN-γ
  • Chemokines: IL-8/CXCL8, IP-10/CXCL10
  • Inflammatory cell infiltrate:
    cell trafficking – chemotaxis;
    neutrophils, macrophages, lymphocytes, mast cells;
    cell activation
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19
Q

What is atopy?

A

A form of allergy in which there is a hereditary of constitutional tendency to develop hypersensitivity reactions (e.g. hay fever, allergic asthma, atopic eczema) 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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20
Q

Is atopy common?

How do allergies vary?

What are the risk factors for developing allergies?

Study These Flashcards
A

Atopy is very COMMON - about 50% in young adults in the UK

Severity varies: Mild occasional symptoms, Severe chronic asthma, Life threatening anaphylaxis

Risk factors = genetic + environmental

21
Q

What are the genetic risk factors for allergies?

Study These Flashcards
A
  • About 80% of atopics have a family history
  • The genetic component is polygenic: 50-100 genes associated with asthma/atopy
  • Genes of the IL-4 gene cluster (chromosme 5) linked to raised IgE, asthma and atopy
  • Genes on chromosome 11q (IgE receptor) are linked to atopy and asthma
  • Genes linked to structural cells are linked to eczema (filagrin) and asthma (IL-33, ORMDL3)
22
Q

What are the environmental risk factors for allergies?

Study These Flashcards
A
  • Age: increases from infancy, peaks in teens, and reduces in adulthood
  • Gender: asthma is more common in males in childhood, and females in adults
  • Family size: more common in small families
  • Infection: early life infections protect
  • Animals: early exposure protects
  • Diet: breast feeding, anti-oxidants and fatty acids protect
23
Q

Give examples of type 1, 2, 4 hypersensitivities

What are they mediated by?

Study These Flashcards
A

Anaphylaxis, urticaria, angioedema: type I hypersensitivity (IgE mediated)

Idiopathic/chronic urticaria: type II hypersensitivity (IgG mediated)

Asthma, rhinitis, eczema: mixed inflammation

  • Type I hypersensitivity (IgE mediated)
  • Type IV hypersensitivity (chronic inflammation)
24
Q

How do allergies develop?

Study These Flashcards
A
  • Development of sensitisation to allergens to sensitise instead of develop tolerance (primary response - usually early in life)
  • Exposure to produce disease (memory response - any time after first exposure)
25
What happens in sensitisation in the development of an allergy?
- T cells are naïve before the have seen the antigen - Once an antigen-presenting cell activates the CD4+ T cells, they then become specific to the presented antigen - They could become Th1 (producing IFN-gamma) - They could become Th2 cells, which leads to the activation of B cells - If the T cell was presented with a harmless antigen, they can become regulatory T cells
26
What is happens during subsequent exposure in development of an allergy?
- The allergens are presented by APCs to the memory Th2 cells - These then cause degranulation of eosinophils by releasing IL-5 - Th2 cells also release IL-4 and IL-13, which stimulate the production of IgE by plasma cells - The IgE then becomes mobilised 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
27
Describe the appearance of eosinophils, what is their amount in the blood and what do they do? Where is it found and where is it made?
- 0-5% of blood leukocytes - Present in blood, most reside in tissues - Recruited during allergic inflammation - Generated from bone marrow - Polymorphus nucleus: two lobes - Contain large granules full of toxic proteins - Lead to tissue damage
28
What do mast cells do, where are they, what do they contain and what do they synthesise?
- Tissue resident cells - They have IgE receptors on cell surface - Cross-linking of IgEs leads to mediator release: - Pre-formed: Histamine, Cytokines, Toxic proteins - Newly synthesized: Leukotrienes, Prostaglandins
29
Describe the appearance of neutrophils, what is their amount in the blood and what do they do? Where is it found and what do they synthesise?
- Important in virus induced asthma, severe asthma and atopic eczema - 55-60% of blood leukocytes - Multi-lobed nucleus - Granules contain digestive enzymes Neutrophils also synthesis: - Oxidant radicals - Cytokines - Leukotrienes
30
Which hypersensitivities is asthma a mix of? | What happens in asthma?
- This is a mixture of type 1 + type 4 - Mast cell activation and degranulation releases histamines (pre-stored mediators) and prostaglandins and leukotrienes (newly synthesised mediators) - These leads to acute airway narrowing
31
What is asthma immuno-pathogenesis (Chronic)? | What are the features?
- This is chronic inflammation of the airways - The lumen of the airway is very narrow and the airway wall is grossly thickened - There will be cellular infiltration of Th2 lymphocytes and eosinophils - Smooth muscle hypertrophy - Mucus plugging - Epithelial shedding - Sub-epithelial fibrosis (if the inflammation has persisted for a long time)
32
What are the importance clinical features of asthma?
- Reversible generalised 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)
33
Allergic rhinitis: seasonal and perennial | Symptoms?
- Seasonal – e.g. hay fever (grass and tree pollens) - Perennial (long term, continuous)– perennial allergic rhinitis (e.g. house dust mites, animal allergens) Symptoms: - Sneezing - Rhinorrhoea - Itchy nose and eyes - Nasal blockage, sinusitis, loss of small/taste
34
What is allergic eczema? Where is it commonly found? What can make it worse? Does it clear?
- Chronic itchy skin rash - Most commonly found in the flexures of the arms and legs - This can lead to house dust mite sensitisation - The house dust mite proteins can get through the dry, cracked skin - Allergic eczema is complicated by bacterial and (rarely) viral infections (e.g. HSV) - 50% clears by 7 years - 90% cleared by adulthood
35
Food allergies - which type of hypersensitivity? | Common ones in infants and children/adults
Type 1 (IgE mediated) hypersensitivity - The common food allergies change with age: Infancy – 3 years: Eggs, cows milk Children/adults: Peanuts, shellfish, nuts, fruits, cereals and soya
36
What are the symptoms of mild and severe food allergies?
Mild reaction: - Itchy lips and mouth - Angioedema - Urticaria Severe reaction: - Nausea - Abdominal pain - Diarrhoea - Anaphylaxis
37
What is anaphylaxis?
- Anaphylaxis = severe generalised allergic reaction - Anaphylaxis is uncommon and potentially fatal - There is generalised degranulation of IgE sensitised mast cells
38
What are the symptoms of anaphylaxis?
- Itchiness around mouth, pharynx and lips - Swelling of the lips, throat and other parts of the body - Wheeze, chest tightness and dyspnoea - Faintness, collapse - Diarrhoea and vomiting - DEATH
39
What is the role of the different body systems in anaphylaxis?
Cardiovascular – vasodilation, cardiovascular collapse Respiratory – bronchospasm, laryngeal oedema Skin – vasodilation, erythema, urticaria, angioedema GI – vomiting and diarrhoea
40
How can allergies be tested?
- Careful history is essential - Skin prick testing - RAST (radio-allergosorbent test) – tests for specific IgE antibodies in the blood - Measure total IgE - Lung function (in asthma)
41
How is anaphylaxis treated?
EMERGENCY treatment: - EpiPen and anaphylaxis kit - Emergency treatment if mild = antihistamine (this can be backed up with a steroid injection) - Emergency treatment if severe=adrenaline
42
How can anaphylaxis be prevented?
- Avoidance of the known allergen - Always carry an anaphylaxis kit and EpiPen - Inform immediate family and caregivers - Wear a MedicAlert bracelet
43
How is allergic rhinits treated?
- Anti-histamines (will help the sneezing, itching and rhinorrhoea if largely type 1 mediated) - Nasal steroid therapy (nasal decongestant) - Cromoglycate (eyes - in children, eyes)
44
What is the treatment for eczema?
- Emollients (maintain the moisture in skin thus reinforcing its barrier function) - Topic steroid cream
45
Asthma treatment - go through the steps if more severe
STEP 1: Use a short-acting beta-2 agonist by inhalation e.g. SALBUTAMOL STEP 2: Inhaled steroid low-moderate dose - Beclomethasone/Budesonide (50-800 mg/day) - Fluticasone STEP 3: Add further therapy - Add long-acting beta-2 agonist or a leukotriene antagonist - High dose inhaled steroids – up to 2 mg/day via a spacer STEP 4: Add courses of oral steroids, SLT, azithromycin - Prednisolone 30 mg/day for 7-14 days - Anti-IgE, Anti-IL4/13, Anti-IL5 mAbs
46
Treatment for severe rhinitis/eczema
Anti-IgE mAb, Anti-IL4/13 mAb, Anti-IL5 mAb
47
What is immunotherapy? | What is it effective for?
- Make people develop tolerance by exposing them to small amounts of the allergen they are allergic to - Effective for single antigen hypersensitivities - E.g. venom allergies (bee or wasp stings), pollens, house dust mites - The antigen used is purified
48
What are the 2 types of immunotherapy? | How long do they take? Where must they be done?
Subcutaneous immunotherapy (SCIT) - 3 years needed (weekly/monthly 2 hr clinic visits) Sublingual immunotherapy (SLIT) - can be taken at home, 2-3 years enough
49
Which 3 process causes airway constriction in asthma?
- Vascular leakage leading to airway wall oedema - Mucus secretion fills up the lumen - Smooth muscle contraction around the bronchi

Year 2 - Immunology (3 decks)

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