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Year 2 - MCD - Immunology > 3 - Hypersensitivity and Allergies (19.02.2020) > Flashcards

3 - Hypersensitivity and Allergies (19.02.2020) Flashcards

1
Q

What should appropriate tolerance occur to?

A

Food, pollens, other plant proteins, animal proteins, commensal bacteria

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2
Q

What does appropriate immune tolerance involve?

A
  • Involves antigen recognition and generation of regulatory T cells and regulatory (blocking) antibody (IgG4) production
  • Antigen recognition in context of “danger” signals leads to immune reactivity, absence of “danger” to tolerance
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3
Q

What are hypersensitivity reactions? What are the different types?

A

Hypersensitivity Reactions occur when immune responses are mounted against

  • Harmless foreign antigens (allergy, contact hypersensitivity)
  • Autoantigens (autoimmune diseases)
  • Alloantigens (serum sickness, transfusion reactions, graft rejection)
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4
Q

What are the different types of hypersensitivity reactions?

A

Classified by Gell & Coombs:

Type I : Immediate Hypersensitivity
Type II : Antibody-dependent Cytotoxicity
Type III : Immune Complex Mediated
Type IV : Delayed Cell Mediated

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5
Q

Examples of Type 1 Hypersensitivity

A

=> immediate

Anaphylaxis
Asthma
Rhinitis
- Seasonal
- Perennial
Food Allergy
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6
Q

Mechanism of Type 1 Hypersensitivity

A

Primary Antigen exposure

  • Sensitisation not tolerance
  • IgE antibody production
  • IgE binds to receptors Mast Cells & Basophils

= IMMEDIATE HYPERSENSITIVITY

Secondary Antigen Exposure

  • More IgE Ab produced
  • Antigen cross-links IgE on Mast Cells/Basophils
  • Degranulation
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7
Q

Mechanism of Type 2 Hypersensitivity

A

Clinical presentation depends on target tissue

  • Organ-specific autoimmune diseases
    - Myasthenia gravis (Anti-acetylcholine R Ab)
    - Glomerulonephritis (Anti-glomerular basement membrane Ab)
    - Pemphigus vulgaris (Anti-epithelial cell cement protein Ab)
    - Pernicious anaemia (Intrinsic factor blocking Abs)

Autoimmune cytopenias (Ab mediated blood cell destruction)

  • Haemolytic anaemia
  • Thrombocytopenia
  • Neutropenia

= ANTIBODY DEPENDANT HYPERSENSITIVITY

Test for specific autoantibodies

  • Immunofluorescence
  • ELISA eg anti-CCP (Cyclic Citrullinated Peptide Abs for Rheumatoid Arthritis)
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8
Q

Mechanism of Type 3 Hypersensitivity

A
  • Formation of Antigen-Antibody complexes in blood
  • Complex deposition in blood vessels/tissue
  • Complement & cell activation
  • Activation of other cascades eg clotting
  • Tissue damage (vasculitis)
    • Systemic lupus erythematosus (SLE)
    • Vasculitides (Poly Arteritis Nodosum, many different types)

IMMUNE COMPLEX MEDIATED HYPERSENSITIVITY

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9
Q

Examples of Type 4 Hypersensitivity

A 
Chronic graft rejection
GVHD
Coeliac disease
Contact hypersensitivity (e.g. nickel)
Many autoimmune diseases….
Asthma
Rhinitis
Eczema
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10
Q

Mechanism of Type 4 Hypersensitivity

A

Three Main Varieties

  • Th1
  • Cytotoxic
  • Th2

Mechanisms

  • Transient/Persistent Ag
  • T cell activation of macrophages, CTLs
  • Much of tissue damage dependent upon TNF & CTLs

=> DELAYED TYPE CELL MEDIATED HYPERSENSITIVITY

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11
Q

What is a common feature of hypersensitivity reactions?

A

Inflammation

  • Immune cell
    - recruitment to sites of injury and/or infection
    - activation
  • Inflammatory mediators – complement, cytokines, etc
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12
Q

What are the features if hypersensitivity reactions?

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

=> Redness, Heat, Swelling and Pain

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13
Q

Which molecules cause increased vascular permeability?

A

C3a, C5a, histamine, leukotrienes

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14
Q

Molecular aspects of inflammation>

A 
Increased vascular permeability
Caused by:- C3a, C5a, histamine, leukotrienes
Cytokines  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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15
Q

What are the key inflammatory cytokines and chemokines?

A

Cytokines: IL-1, IL-6, IL-2, TNF, IFN-γ

Chemokines: IL-8/CXCL8, IP-10/CXCL10

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16
Q

CXCL - what do these molecules do?

A

recruit leukocytes usually

chemokines

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17
Q

Genetic risk factors for allergy

A

~80% of atopics have a family history

Polygenic

  • 50-100 genes linked to asthma/atopy
  • genes of IL-4 gene cluster (chromosome 5) linked to raised IgE, asthma, atopy
  • genes on chromosome 11q (IgE receptor) linked to atopy and asthma
  • genes linked to structural cells linked to eczema (filaggrin) and asthma (IL-33, ORMDL3, CDHR3)
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18
Q

Severity levels of allergic reactions

A

mild occasional symptoms
severe chronic asthma
life threatening anaphylaxis

19
Q

Is allergy common?

A

yes

  • prevalence of atopy is 50% in young adults in UK
20
Q

Environmental risk factors for allergy

A
  • Age - increases from infancy, peaks in teens, reduces in adulthood
  • Gender - asthma more common in males in childhood, females in adults (sex hormones play a role but it is not yet understood)
  • Family size - more common in small families (also e.g. first born is more likely to get allergy than a e.g. 6th born)
  • Infections - early life infections protect
  • Animals - early exposure protects
  • Diet - breast feeding, anti-oxidants, fatty acids protect
21
Q

What are the different types of inflammation in allergy?

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)
22
Q

What is required to express allergy as a disease?

A
  • Development of sensitisation to allergens instead of tolerance (primary response - usually in early life)
  • Further allergen exposure to produce disease (memory response - any time after sensitisation)
23
Q

What happens in sensitisation to an antigen in atopic airway disease?

A
  • inhaled antigen
  • taken up by dendritic cells lining the airway
  • dendritic cells process protein into peptides and presents these to CD4+ T-cells
  • T-cell can develop into
    • Th1
    • Th2
    • Treg
  • in allergy the Th2 cell is the dominant pathway (in developing sensitisation rather than tolerance)
  • produce IL-4 and IL-13
  • this causes B-cell proliferation and differentiation (to plasma cells)
  • B-cells make IgE antibodies (due to stimulation by T-helper cells with IL-4 and IL-13
24
Q

What happens during a subsequent exposure to an antigen in atopic airway disease?

A
  • dendritic cells take up antigen and process it into peptiedes
  • present peptides to memory T-cells
  • these produce IL-4 and IL-13
  • B-cells incl. plasma cells make antibodies (IgE)
  • IL-5 also secreted by Th2 cells: causes recruitment of eosinophils
  • this leads to inflammation (eosinophilic)
  • there is also mast-cell and t-cell mediated inflammation

-> all this occurs as a memory response.

25
Q

Neutrophils

A
  • Important in
    • virus induced asthma
    • severe asthma
    • atopic eczema
  • 55-70% of blood leukocytes
  • Polymorphonuclear cells (PMNs)
    • nucleus contains several lobes
  • Granules contain
    • digestive enzymes
  • Also synthesize
    • oxidant radicals
    • cytokines
    • leukotrienes
  • Most common Leukocytes
26
Q

Immunopathogenesis of asthma

A

Acute inflammation of the airways

  • mast cell activation & degranulation
    • Pre stored mediators
      • histamine
    • Newly synthesised mediators
      • prostaglandins, leukotrienes
  • Acute airway narrowing

Chronic inflammation of the airways

  • Cellular infiltrate
    • Th2 lymphocytes, eosinophils
  • Smooth muscle hypertrophy
  • Mucus plugging
  • Epithelial shedding
  • Sub epithelial fibrosis
27
Q

What is the rsponse pattern to allergens?

A
  • there is an early response
  • goes back to baseline
  • there is a weaker late response some hours later.
28
Q

Important clinical features of asthma

A
  • Reversible generalised airway obstruction
  • Chronic episodic wheeze
  • Bronchial hyperresponsiveness
  • Bronchial irritability
  • Cough
  • Mucus production
  • Breathlessness
  • Chest tightness
  • Response to treatment
  • Spontaneous variation
  • Reduced & variable peak flow (PEF
29
Q

What is allergic rhinitis?

A
  • Seasonal - hay fever - grass, tree pollens
  • Perennial - perennial allergic rhinitis
    • HDM, pets
  • Symptoms
    • sneezing
    • rhinorrhoea
    • itchy nose, eyes
    • nasal blockage, sinusitis, loss of smell/taste
30
Q

Allergic eczema

A
  • Chronic itchy skin rash
  • Flexures of arms and legs
  • HDM sensitisation and dry cracked skin
  • Complicated by bacterial and (rarely) viral infections (early childhood, herpes simplex)
  • 50% clears by 7 years
    90% by adulthood
31
Q

Food allergy

A

Infancy-3yrs: egg, cows milk

Children/adults: peanut, nuts, shell fish, fruits, cereals, soya

Mild
-> Itchy lips, mouth, angioedema, urticaria

Severe
-> Nausea, abdominal pain, diarrhoea, collapse, wheeze
Anaphylaxis

32
Q

What is anaphylaxis?

A
  • Anaphylaxis: severe generalised allergic reaction
  • Uncommon, potentially fatal
  • Generalised degranulation of IgE sensitised mast cells
33
Q

What body systems are involved in anaphylaxis?

A

Cardiovascular - vasodilatation, cardiovascular collapse

Respiratory - bronchospasm, laryngeal oedema

Skin - vasodilatation, erythema, urticaria, angioedema

GI - vomiting, diarrhoea

34
Q

Symptoms of anaphylaxis

A
  • itchiness around mouth, pharynx, lips
  • swelling of the lips, throat and other parts of the body
  • wheeze, chest tightness, dyspnoea
  • faintness, collapse
  • diarrhoea & vomiting
  • death if severe & untreated
35
Q

Symptoms of anaphylaxis

A
  • itchiness around mouth, pharynx, lips
  • swelling of the lips, throat and other parts of the body
  • wheeze, chest tightness, dyspnoea
  • faintness, collapse
  • diarrhoea & vomiting
  • death if severe & untreated
36
Q

Investigations and diagnosis of allergies?

A
  • Careful history essential
  • Skin prick testing
  • RAST (blood specific IgE): Radioallergosorbent test
  • Total IgE
  • Lung function (asthma)
37
Q

How do you treat anaphylaxis?

A

Emergency Treatment

  • EpiPen & Anaphylaxis kit
  • antihistamine, steroid, adrenaline
  • Seek immediate medical aid!!

Prevention

  • Avoidance of known allergen
  • Always carry a kit & EpiPen
  • Inform immediate family & caregivers
  • Wear a MedicAlert® bracelet
38
Q

How do you treat allergic rhinitis and eczema?

A

Allergic rhinitis

  • anti-histamines (sneezing, itching, rhinorrhoea)
  • nasal steroid spray (nasal blockage)
  • cromoglycate (children, eyes)

Eczema

  • emollients
  • topical steroid cream

If severe
anti-IgE, anti-IL-4/-13, anti-IL-5 mAb

39
Q

Steps in asthma treatment

A

Step 1. Use short acting b2 agonist drugs as required by inhalation -> Salbutamol

Step 2. Inhaled steroid low-moderate dose
Beclomethasone/budesonide (50-800mg per day)
Fluticasone (50-400mg per day)

Step 3. Add further therapy
Add long acting bronchodilators, leukotriene antagonist
High dose inhaled steroids - up to 2mg per day via a spacer

Step 4. Add courses of oral steroids, SLIT, azithromycin
Prednisolone 30mg daily for 7-14 days
Anti-IgE, anti-IL-5, anti-IL-4/-13 monoclonal Abs

40
Q

SLIT

A

sublingual immunotherapy

41
Q

Immunotherapy in allergies

A

Effective for single antigen hypersensitivities

  • Venom allergy - bee or wasp stings
  • Pollens
  • HDM (house dust mites)
  • Antigen used is purified

Subcutaneous immunotherapy (SCIT)

  • 3 years needed
  • Weekly/monthly 2hr clinic visits

Sublingual immunotherapy (SLIT)

  • Can be taken at home
  • 3yrs needed
42
Q

Immunotherapy in allergies

A

Effective for single antigen hypersensitivities

  • Venom allergy - bee or wasp stings
  • Pollens
  • HDM (house dust mites)
  • Antigen used is purified

Subcutaneous immunotherapy (SCIT)

  • 3 years needed
  • Weekly/monthly 2hr clinic visits

Sublingual immunotherapy (SLIT)

  • Can be taken at home
  • 3yrs needed
43
Q

What are the important cell types in allergy?

A
  • eosinophils
  • mast cells
  • neutrophils

Year 2 - MCD - Immunology (5 decks)

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