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Year 2 MCD Immunology > 3: Hypersensitivity and Allergy > Flashcards

3: Hypersensitivity and Allergy Flashcards

1
Q

What are hypersensitivits immune reactions?

A

They 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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2
Q

What are alloantigens?

A

Thy are non-self antigens from members of the same species (e.g. blood group antigens, tissue antigens)

–> If reaction against alloantigens: also hypersensitivity

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3
Q

What are the different types of hypersensitivity reactions?

A

There are 4 types, classified by the way they act/are mediated

  • Type I : Immediate Hypersensitivity
  • Type II : Antibody-dependent Cytotoxicity (insoluble antigens)
  • Type III : Immune Complex Mediated (soluble antigens)
  • Type IV : Delayed Cell Mediated
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4
Q

Name some conditions that are meditated via a Type I hypersensitivity response

A

Type I= immediate response e.g.in

  • Anaphylaxis
  • Ashmah
  • Rhinitis
    • seasonal
    • perenial
  • Food allergy
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5
Q

What is required for a Type I hypersensitivity reaction?

A

Before Type I hypersensitivity can happen: Sensitisation required

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6
Q

Explain the process of sensitisation prior to a Type I hypersensitivity response

A

!Type I is first and fast.

  1. Body comes into contact with antigen –> engulfed and presented on B-cells
  2. T-cell activated presenting B-cell and induces class switching and IgE antibody production (by plasma cell)
  3. Produced IgE antibodies against antigen become resident on Mast cells and Basophils (with constant region)
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7
Q

Explain the process at the 2nd exposure to an antigen in Type I hypersensitivity

A
  1. Antigen binds to IgE on Mast cells/Basophils
  2. Binding causes cross-linking of surface IgE antibodies
  3. Leading to activation of Mast cells –>
    1. Degranulation and release of
      1. Hisamine
      2. Prostaglandin D2 and
      3. Heparin (+more)
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8
Q

Explain the mechanism in Type II hypersensitivity

A

Type II= antibody dependant cell mediated cytotoxicity (Type II is cy-2-toxic.)

  • IgG or IgM antibodies bind to tissue-specific (cell specific) antigens (–> on normal cell surfaces, bind to non-soluble antigens)
  • Leading to
    • complement acitvation and destruction of cell
    • Attraction of more cytotoxic cells
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9
Q

Name some conditions that are mediated via a Txpe II hypersensitivity response

A

Often they are organ specific (= antibodies against organ-specific antigens are produced), leading to

  • Graves disease
  • Pernicious anaemia (due to destruction of Intrinsic factor and therfore B12 deficiency)
  • Myasthenia Gravis
  • Autoimmune cytopenias (in blood)
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10
Q

Explain a Type III hypersensitivity reaction

A

!: Type III means three things stuck together: antigen + antibody + complement

  • Soluble (free) antigen-antibody (IgG) complexes form in the blood stream
  • Deposit of immune comlexes on vascular walls
  • If so: complement system gets activated and recruits neutrophils
  • Neutrophils bind to antigen and get activated resulting in release of destructive substances
  • Leading to: Endothelial cell and BM damage
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11
Q

Name examples of a condition that are associated with a type III hypersensitivity reaciton

A

SLE

Systemic lupus erythematosus

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12
Q

Name examples of conditions that are Type IV hypersensitivity mediated

A

Type IV= delayed

4 Ts associated with the type IV hypersensitivity: T cells, Transplant rejection, TB skin tests, Touching (contact dermatitis).

  • chronic grapht rejection
  • Contact hypersensitivity
  • coeliac disease
    • All Th1 mediated
  • Asthmah/Rhinits, Eczema
    • Th2 mediated
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13
Q

Explain the process of Type IV hypersensitivity

A

It is T-cell mediated and delayed leading to Hypersensitivity

Both CD4+ and CD8+ cells are important

  • CD4+
    • Antigen is presented on APC (MHC II)
    • CD4+ bind to it and releases chemokines and cytokines e.g.
      • IL-2: recruits more T-cells
      • IF-gamma: recruits macrophages (Th1)/ (eosinophils in Th2) and triggers inflammatory responst
  • CD8+
    • bind to antigen presented on MHC I and lead to cellular destruction
  • –>Leading to Inflammation and tissue damage
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14
Q

What are the features of inflammation?

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

Leading to:

  • Redness
  • Heat
  • Swelling
  • Pain
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15
Q

What do all types of hypersensitivity have in common?

A

The inflammation, characterised by

  1. Immune cell recruitement and activation
  2. release of inflammatory mediators
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16
Q

What might cause the development of allergy?

A

There are genetic and environmental risk factors

  • Genetic
    • polygenic, many are associated with having an increased risk (there is some predisposition)
  • Environmental
    • Exposure to many antigens/infections seems to be preventative
      • big families
      • early exposure to animals
    • Age (peak in teens)
    • gender (asthmah more common in male inchidhood, females in adulthood)
    • diet
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17
Q

What is the difference betwenn hypersensitivity and allergy?

A

Hypersensitivity reaction: a condition in which the normally protective immune system has a harmful effect on the body

Allergy: an abnormal immunological response to an otherwise harmless environmental stimulus (e.g., food, pollen, animal dander)

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18
Q

What are the different types of inflammation that can occur in allergy?

A

It can by Type I(IgE mediated), Type II and IV (IgG mediated) or a combintaiton of two

  • 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)
19
Q

What is needed before someone can develop an allergy?

A

Sensitisation to allergens required (insted or tolerance)

20
Q

Explain the process of sensitisation in allergy

A

Before one can be allergic to sth, one first need to be sensitized

  1. APC present antigen to CD4+ T-cell
  2. differentiated into (memory) Th2
  3. activation of B-lymphocytes (via IL-4/13)
    1. Class switch and production of IgE
21
Q

What happens to subsequent exposure to an antigen in allergy?

A
  1. Allergen is presented to Th2 cells
  2. set of an inflammatory response
    1. recruit eosinophils via IL-5
    2. And B-cells via IL-4 + IL-13
      1. IgE on mast cells+ antigen binding causes the activation of mast cells
22
Q

What is the role of eosinophils in allergic responses?

A

0-5% of immune cells, bilobular with many granules

  • Recruited during allergic inflammation (mainly residue in tissues)
  • Generated from bone marrow
  • Contain large granules with toxic proteins
    • release Leads to tissue damage
23
Q

Explain the role of Mast cells in inflammation

A
  • Tissue resident cells
  • IgE receptors on cell surface
  • Crosslinking of IgEs leads to
  • Mediator release
    • Pre-formed
      • histamine
      • cytokines
      • toxic proteins
    • New synthesation of mediators
      • leukotrienes
      • prostaglandins
24
Q

Explain the role of neutrophils in allergy

A
  • Important in
    • virus induced asthma
    • severe asthma
    • atopic eczema
  • Granules contain
    • digestive enzymes
  • Also synthesize
    • oxidant radicals
    • cytokines
    • leukotrienes
25
Q

Explain the pathophysiology of astmah

A

Asthmah= acute and chronic inflammation of the ariway

  1. Acute (Type I, IgE)
    • leading to mast cell activation and degranulation (relaese of histamine, prostaglandins and leukotrins)
    • and thereby acute airway narrowing
  2. Chroinc inflammation (Type IV)
    • cellular inflitration of Eosinophils and Th2 in airway
    • SM hypertrophy
    • Mucus plugging
    • epithelial shedding
    • sub-epithelial fibrosis
26
Q

Which factors contribute to the acute narrowing of the airway in astmah?

A
  1. Oedema
    1. due to increased vascular leakage
  2. Mucus secretion and
    1. also due to increased vascular leakage
  3. Bronchospasm (SM contraction)
27
Q

What are the important clinical features of astmah?

A
  • Reversible generalised airway obstruction
    • Chronic episodic wheeze
  • Bronchial hyperresponsivenes and irritability
  • Mucus production
    • Cough
  • Breathlessness, Chest tightness
  • Response to treatment
  • Spontaneous variation
  • Reduced & variable peak flow (PEF)
28
Q

What are the symptoms of allergic rhinitis?

A
  • sneezing
  • rhinorrhoea
  • itchy nose, eyes
  • nasal blockage, sinusitis, loss of smell/taste
29
Q

What are the two forms of allergic rhinitis?

How do they differ?

A

Differn in the time that the stimulus to allergy is there:

  • Seasonal - hay fever - grass, tree pollens
  • Perennial - perennial allergic rhinitis
    • äHDM, pets
30
Q

What type of hypersensitivitsy is allergic Rhinits?

A

Type I

31
Q

Explain the characteristics and symptoms of allergic eczema

A
  • Chronic itchy skin rash, dry cracked skin
    • Expecially in Flexures of arms and legs
  • HDM (house dust mite) sensitisation and dry cracked skin
  • Complicated by bacterial and (rarely) viral infections (early childhood, herpes simplex)
  • 50% clears by 7 years
  • 90% by adulthood
32
Q

What are the most commonest types of food allergies in child and adulthood?

A
  • <3 years: Egg and Cows Milk
  • In adulthood: peanut, nuts, shell fish, fruits, cereals, soya
33
Q

What are the characterisitcs of a mild food allergy?

A
  • Itchy lips, mouth,
  • angioedema,
  • urticaria
34
Q

What are the characteristics of a severe food allergy?

A
  • Nausea, abdominal pain, diarrhoea, collapse, wheeze
  • Anaphylaxis
35
Q

What is anaphylaxis?

A
  • Anaphylaxis: severe generalised allergic reaction
  • Uncommon, potentially fatal
  • Generalised degranulation of IgE sensitised mast cells
  • –> Type I hypersensitivity
36
Q

What are the 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
37
Q

What happens in anaphylaxis with the

  • CVS system
  • Respiratory system
  • Skin
  • and GI system
A
  • Cardiovascular - vasodilatation, cardiovascular collapse
  • Respiratory - bronchospasm, laryngeal oedema
  • Skin - vasodilatation, erythema, urticaria, angioedema
  • GI - vomiting, diarrhoea
38
Q

How would you investigate /diagnose someonw with allergy?

A
  1. History taking
  2. skin prick test
  3. RAST (blood specific IgE): –> like skin prick test but outside body
  4. total IgE
  5. Lung function (for astmah)
39
Q

How do you treat anaphylaxis?

A

EpiPen & Anaphylaxis kit

  • antihistamine, steroid, adrenaline
  • Seek immediate medical aid
40
Q

Explain the treatment of allergic rhinitis

A

Depending on the severity of the disease

Allergic rhinitis

  1. anti-histamines (sneezing, itching, rhinorrhoea)
  2. If more severe: nasal steroid spray (nasal blockage)

cromoglycate (children, eyes) (don’t know what it does)

41
Q

How do you treat allergic eczema?

A
  1. emollients
  2. topical steroid cream
42
Q

How could you treat severe cases of allergic eczema or allergic rhinitis?

A

With immunotherapy

  • e.g. anti-IgE, anti-IL-4/-13, anti-IL-5 mAb
43
Q

How do you treat Astmah

A

Depending on severity

  1. ß2 agonist in acute attacks
  2. . Inhaled steroid low-moderate dose
  3. Add long acting bronchodilators, leukotriene antagonist, High dose inhaled steroids
  4. Add courses of oral steroids, SLIT, azithromycin + monochlonal antibodies
44
Q

Explain the concept of immunotherapy in the treatment of hypersensitivities

A

Can be used for single-allergen allergies

–> The antigen is extracted and purified and given as

  • SC
  • or SUb-lingual

–> over 3 years, train the immune system to tolerate antigens

Year 2 MCD Immunology (6 decks)

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