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204- Immunology > Atopy, allergy and delayed type hypersensitivity > Flashcards

Atopy, allergy and delayed type hypersensitivity Flashcards

1
Q

Define the early phase allergic reaction

A
  • exposure to allergens leads to rapid development of symptoms in allergic individual
  • develops withins seconds/minutes as allergens bind to preformed IgE on surface of mast cells and basophils
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2
Q

Explain how the early phase allergic reaction happens

A

IgE bind to specific allergen
Cross linking of IgE by allergen leads to clustering of Fc3R1 receptors. The intracellular portion of recptor is phosphorylated –> intracellular cascade –> cellular activation –> mast cell degranulation releasing histamine, tryptase and other preformed mediators

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3
Q

What are leukotrienes

A

Delayed mediators pharmacologically similar to histamine

Its effects

  • skin: wheal and flare
  • nose: discharge, sneezing
  • eyes: conjunctivitis
  • lung: wheeze
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4
Q

State the effects of mast cell activation and degranulation on

  1. GIT
  2. Airway
  3. Blood vessels
A
  1. expulsion of GIT contents by diarrhoea, vomit
  2. congestion and blockage of airways; swelling and mucus production in nasal passages
  3. increased fluid in tissues causing increased flow of lymph to nodes, increased cells and protein in tissues and increased effector responses in tissues
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5
Q

What is the source of allergen antigens?

A

Almost always innocuous environmental proteins

- pollens, housedust mite faeces, stinging insect venom

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6
Q

Describe the general characteristics of allergens

What are the physical properties that favour transition across mucus membranes?

Why is this important?

Why is homology relevant?

A
  • All proteins- only proteins can produce a T cell (and therefore B cell) response
    (most are biologically active, enzymes. Could be coincidental)
  • soluble, LMW
  • need to cross mucus membranes to activate immunity
  • Low homology wont bind MHC, high homology wouldve been deleted during negative selection. Therefore allergens must have intermediate homology
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7
Q

What is anaphylaxis?

What happens?

What are the commonest triggers in the UK?

A

Generalised allergic reaction

Systemic release of histamine causes generalised vasodilation and fluid loss from circulation to tissues

  • Cutaneous: hives, angiodema
  • Gut histamine release: laryngeal oedema, bronchoconstriction
  • Circulation: vasodilation, hypotension
  • Food, drugs, insect venom
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8
Q

What are the cardinal features of anaphylaxis

A
  • Typical symptoms: hives, angioedema, laryngeal oedema, bronchoconstriction, hypotension
  • multisystem and dramatic
  • rapidly follows exposure to allergen
  • improves quickly
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9
Q

Describe oral allergy syndrome

A
  • most common allergy
  • IgE directed pollen proteins cross react with homologous proteins in plant derived foods
  • Oral itching upon exposure to raw fruit, nuts and vegetables
  • In the UK: pollen (mainly birch) and food (mainly rosaceae fruits)
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10
Q

Rhinitis and lower airway obstruction are types of airway disease. Describe them.

Exposure to allergens can be seasonal or episodic. Give examples

What happens if the symptoms are chronic?

A

Rhinitis: sneezing, rhinorhoea, blockage due to type 1 allergy
Lower airway obstruction: wheezing due to type 1 allergy

Seasonal: pollen, moulds
Episodic: occupational, animal dander

If symptoms are chronic, the inflammation becomes established ad cannot be explained in terms of mast cell degranulation

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11
Q

What is meant by the immunological tightrope?

A

The immune system must strike a balance between

Activation: required for defence against infection and cancer

Tolerance: required to prevent autoimmunity and inflammatory diseases

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12
Q

What are the origins of allergic disease?

A

allergic/atopic march = progression of disease from infancy
- most children will outgrow eczema and food allergies
(rhinitis and asthma may not be outgrown)

de nova presentation in adults

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13
Q

Describe symptom progression of asthma, sensitisation, histopathology and comment on the application of early phase reaction as an explanation of asthma

A
  • ongoing symptoms
  • most patients are sensitised to a variety of airborne allergens
  • biopsy shows inflammatory infiltrate and airway changes (REMODELLING) such as thickened basement membrane and smooth muscle hyperplasia
  • early phase reaction doesnt provide good explanation
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14
Q

Describe the late phase allergic reaction

A
  • develops after some hours

- biopsy shows infiltration with inflammatory cells: CD4 T cells, eosinophils, mast cells

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15
Q

T helper cells and Treg are CD4+ cells.

Which cytokines are produced from TH1, TH2, TH17 and Treg

A

Th1 –> IFN-y
Th2–> IL4,5,9,13
Th17 –> IL17
Treg –> IL10, contact dependent mechanisms

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16
Q

Which cytokines are important in allergic disease?

A
  • Allergic inflammation is rich in T cells expressing Th2 cytokines

IL4 is required for B cell class switch to IgE
IL13: bronchial hyperesponsiveness
IL4 and IL13 promotes mucus hypersecretion
IL5 required for eosinophil survival and recruitement
IL9 recruits mast cells

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17
Q

Differentiate between the role of acute and chronic responses in asthma

A

Acute responses: inflammatory mediators cause an increase in mucus secretion and smooth muscle contraction –> airway obstruction, recruitement of cells from circulation

Chronic responses: caused by cytokines and eosinophils products. Activated Th2 cells and other inflammatory cells accumulate and products of Th2 lead to chronic disease
(IL4,5,9,13)

18
Q

Describe how genetics is a potential factor in the aetiology of allergy

A
  • childhood allergy strongly predicted if parents have allergies
  • numerous genetic Rx factors identified

BUT…. doesnt explain epidemic

19
Q

Describe how hygiene hypothesis (Strachan 1989) is a potential factor in the aetiology of allergy

A
  • In westernised countries there are SMALL family sizes, AFFLUENT/URBAN homes, STABLE instestinal microflora, HIGH ANTIBIOTIC use, low/absent HELMINTH burden, good sanitation, low OROFAECAL burden
  • This promotes allergic disorders
  • Low hygiene levels and high pathogen load, helminth infection skews immunity from Th2 to Th1 and induces Treg.
20
Q

Describe the process involved in a SKIN TEST and what it is used for

  • Indication
A

Used to detect allergen-specific IgE in vivo. Indicated if patient history suggestive of IgE-mediated allergy

  1. Allergen extract applied as drops
  2. Top layer of epidermis punctured with lancet
  3. WHEAL AND FLARE response after 15 minutes = positive result
    * needs interpretation in clinical context
21
Q

Describe the process involved in a RAST and what it is used for

A

Type of ELISA used to detect allergen-specifc IgE in vivo

  1. Patient serum incubated in well coated with purified allergen
  2. IgE in sera of sensitised patient binds allergen
  3. Immobilised IgE antibodies detected with polyclonal anti-IgE detection antibody
22
Q

Pure symptoms relievers are used in treatment of allergy

NASAL DECONGESTANTS

  • example
  • MOA
  • Route of administeration
  • Period of use
A
  • Oxymetazoine
  • Vasoconstriction via a1 adrenoreceptors
  • Topical and systemic
  • Short term use
23
Q

Pure symptoms relievers are used in treatment of allergy

SALBUTAMOL

  • class of drug
  • MOA
A
  • B2 agonist

- Smooth muscle relaxation via B2 adrenoreceptors on lung

24
Q

Pure symptoms relievers are used in treatment of allergy

EPINEPHRINE
- MOA

A
  • Oppose vasodilation and bronchoconstriction via systemic adrenergic effects
25
Q

Drugs acting on early phase mediators can be used in treatment of allergy

  1. MAST CELL STABILISERS
    - example
    - MOA
    - Pharmacokinetics
    - ADV/D.ADV
A
  • Sodium cromoglycate
  • Reduces mast cell degranulation by unknown mechanism
  • Not orally active, topically used
  • Short 1/2 life –> frequent dosing
  • Adv: Steroid free; Dadv: poor efficacy
26
Q

Drugs acting on early phase mediators can be used in treatment of allergy

  1. H1 antihistamines
    - 1st and 2nd gen example
    - MOA
    - Side effects
A
  • Best used BEFORE exposure to allergen
  • MOA: inverse agonist at H1 histamine receptor

1st GEN

  • Chlorpheniramine
  • Considerable sedation, drug interactions

2nd GEN

  • Cerizine, Orathidine, Desloratidine, Fexofenadine
  • No/minimal sedation, 1/day
27
Q

Drugs acting on early phase mediators can be used in treatment of allergy

  1. Leukotriene receptor antagonists
    - example
    - efficacy
    - advantages
A
  • Montelukast
  • Inferior to antihistamines at decreasing early allergic responses
  • Beneficial in chronic asthma
28
Q

Corticosteroids can be used in treatment of allergy

Outline their MOA

How does this MOA reflect in dosing?

A
  1. Steroid receptor bound to HSP90(heat shock protein) in cytosol
  2. Steroid crosses cell membrane binds receptor releasing HSP90
  3. Steroid:receptor complex crosses nuclear membrane and binds specific gene regulatory sequences –> transcription

This occurs in T/B cells and innate immune cells

Steroids have delayed onset of action and must be taken regularly

29
Q

Corticosteroids can be used in treatment of allergy

Give an exmaple of a corticosteroid that can be taken via nasal route, inhaled, topical route

How else can they be administered?

A

NASAL- beclamethason, momethasone, fluticasone

INHALED- beclamethasone, fluticasone

TOPIC- hydrocortisone
** may cause local and system side effects

Ophthalmic drops

30
Q

Omalizumab can be used to treat allergies

What is it?

Outline its MOA’s

A

Monoclonal antibody directed against IgE used for atopic asthma

  • decreases cell bound IgE availability by binding it
  • decreases expression of high affinity receptors
  • decreases mediator release
  • decreases allergic inflammation, prevents exacerbation of asthma and decreases symptoms
31
Q

Allergen specific immunotherapy can be used to treat allergies

How is this done?
- MOA
Give an advantage

A
  • Allergen doses administered subcutaneously or sublingually
  • This induces Treg responses to allergen, decreases Th2 responses, induces allergen-specific IgG antibodies, decreases mast cell responsiveness
  • Provides long term protection
32
Q

What immune component is responsible for type IV delayed hypersensitivity?

Contact dermatitis is an example of this. What are its sensitising agents and how do they provoke an immune response

A

Antigen specific effector T cells

Sensitising agents: highly reactive small molecules capable of penetrating skin

  • React with self proteins forming a protein hapten which is picked up by Langerhan cells which migrate to regional lymph nodes
  • Langerhan cells process and present antigen via MHC2
  • Complex recognised as foreign and activated T cells migrate to dermis
33
Q

Describe the process of elicitation in contact dermatitis

A

Chemokines recruit macrophages which process antigen stimulating Th1 which secretes IFN-y and TNFa and TNFb

34
Q

What is the role of IFN-y and TNFa/b?

A

IFNy increases expression of vascular adhesion molecules, activated macrophages

TNFa/b cause local inflammation

35
Q

How does poison ivy lipid (pentadecacatechol) cause contact dermatitis?

A

May cross the skin of susceptible individuals and modify extracellular proteins

36
Q

Describe the patch test used for contact dermatitis

  • indication
  • method
  • positive result
A
  • Hx suggestive of contact dermatitis
  • Antigen-impregnated patch placed on back and left for 2 days
  • Eczematous reaction
37
Q

Address the following parameters in respect to type 1 hypersensitivity

  • Clinical features
  • Temporal aspects
  • Causative agents
  • Effector MOA
  • Assessment
  • Management
A
  • Features consistent with mast cell degranulation (hives, low bp, dyspnoea, swelling, severe diarrhoea
  • Quickly follows exposure to agent then improves
  • Naturally occurring proteins
  • Allergen-specific IgE, mast cell degranulation
  • Allergy clinic (Hx, skin prick test, serology for IgE)
  • Avoidance, pharmacotherapy, immunotherapy
38
Q

Address the following parameters in respect to type 4 hypersensitivity

  • Clinical features
  • Temporal aspects
  • Causative agents
  • Effector MOA
  • Assessment
  • Management
A
  • Eczematous skin reaction
  • Delay between exposure and symptoms
  • Varies, synthetic molecules
  • Antigen-specific effector Th1 cells
  • Dermatology clinic (UK), allergy clinic (EU), Hx, Patch test
  • Avoidance
39
Q

What is the tuberculin skin test?

  • aim
  • method
  • positive result
  • limitation
A
  • to determine EXPOSURE to MTB
  • Tuberculin (complex mix of MTB antigens) injected intradermally
  • Local inflammatory response over 24-72 hours
  • Poor test for acute TB as in active TB
40
Q

Describe the immunological process that lead to a positive result in the TST

A

Antigen processed by local APC

Th1 effector cell recognises antigens and releases cytokines which act on vascular endothelium

Recruitment of phagocytes and plasma to site of injection produces a visible lesion

41
Q

Outline how we can detect the presence of TB-specific Th1 cells in vitro by IGRA

  • What is it?
  • How is it performed?
  • Why is it only effective on latent TB infection?
A

Blood sample taken to assess latent TB infection by IGRA

  • patient blood incubated with TB antigens (CFP10 and ESAT6). Mixture is then centrifuges so that cells form a pellet. Supernatant is removed by pipetting leavinh behind pellet. Supernatant is then analysed for IFN-y concentration by ELISA
  • Bound to well is Anti-IFNy; add supernatant; add labelled antibody against IFN-y

In active TB, naive t cells have recognised MTB thus becoming effector T cells however this wont be in circulation yet

204- Immunology (16 decks)

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