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Year 5 Path Immunology > Year 2: Hypersensitivity and Allergy > Flashcards

Year 2: 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

What is the laboratory definition of sensitisation?

A

Detection of IgE antibodies either by skin prick test or in vitro blood test

(Does not have to correspond to clinical symptoms of allergy)

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7
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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8
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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9
Q

What is the time-frame in which a Type I hypetsensitivity reaction occurs?

A

Initial release will happen within 4h

However, anaphylaxic can be biphasic with 2nd peak occuring within 72h (usually 10h)

(Therefore clinically monitor for 6-12h after treatment, depending on how well the response to initial treatment was)

Admit children under 16 with anaphylaxis

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10
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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11
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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12
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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13
Q

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

A

SLE
* Polyarteritis nodosa

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14
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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15
Q

Name some examples of Type IV hypersensitivity reactions

A
  1. Type 1 DM
  2. MS
  3. Rheumatoid arthritis (also a type III)
  4. Contact termatitis
  5. Mantoux test
  6. Crohn’s disease
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16
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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17
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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18
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
19
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
20
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)

21
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)
22
Q

What is needed before someone can develop an allergy?

A

Sensitisation to allergens required (insted or tolerance)

23
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
24
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
25
What is the role of eosinophils in allergic responses?
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
26
Explain the role of Mast cells in inflammation
* 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
27
Explain the role of neutrophils in allergy
* Important in * virus induced asthma * severe asthma * atopic eczema * Granules contain * digestive enzymes * Also synthesize * oxidant radicals * cytokines * leukotrienes
28
Explain the pathophysiology of astmah
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
29
Which factors contribute to the acute narrowing of the airway in astmah?
1. Oedema 1. due to increased vascular leakage 2. Mucus secretion and 1. also due to increased vascular leakage 3. Bronchospasm (SM contraction)
30
What are the two forms of allergic rhinitis? How do they differ?
Differn in the time that the stimulus to allergy is there: * Seasonal - hay fever - grass, tree pollens * Perennial - perennial allergic rhinitis * äHDM, pets
31
What type of hypersensitivitsy is allergic Rhinits?
Type I
32
Explain the characteristics and symptoms of allergic eczema
* 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
33
What are the most commonest types of food allergies in child and adulthood?
* \<3 years: Egg and Cows Milk * In adulthood: peanut, nuts, shell fish, fruits, cereals, soya
34
What is anaphylaxis?
* Anaphylaxis: severe generalised allergic reaction * Uncommon, potentially fatal * Generalised degranulation of IgE sensitised mast cells * --\> Type I hypersensitivity
35
How would you investigate /diagnose someonw with allergy?
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)
36
Explain the concept of immunotherapy in the treatment of hypersensitivities
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
37
What allergic diseases usually don't present until adulthood?
1. Drug allergy 2. Bee allergy 3. Oral allergy syndrome 4. Occupational allergy
38
What are some of the clinical features of igE mediated allergic responses?
1. at least 2 organ systems involved 2. reproducible 3. triggered by co-factors (exercise, alcohol)
39
What is the use of skin prick test in the diagnosis of allergy?
* Useful to confirm clinical history. Negative test excludes IgE-mediated allergy * But positive does not equal allergy (only shows sensitisation), needs clinical history to confirm allery * Positive control = histamine, negative control = dilutant
40
What is RASt test? How should the results be interpreted?m
Quantitative specific IgE to putative allergen (RAST) * Measure levels of IgE in serum against a particular allergen (e.g. peanut) * Confirms dx of allergy and monitors response to anti-IgE treatment * Less sensitive/specific than skin prick testing
41
What is Component-resolved diagnostics?
This test measures the IgE response to a specific allergen protein (whilst conventional tests measure response to range of allergen proteins) E.g. peanuts contain at least 5 major allergens: 2. Ara h 2 – High risk anaphylaxis to peanut and nuts 3. Ara h 8 – Localised oral reactions to peanut and stone fruit only
42
What is the gold-standard test for diagnosis of allergy?
**Challenge Test** * Double-blind oral food challenge is gold standard for food allergy BUT risk of severe reaction when testing. * Increasing volumes of offending food/drug are ingested under close supervision.
43
How is a laboratory diagnosis of anaphylaxis made?
Serial mast cell tryptase (at 30min-2h, 2h and 24h) As usuall peak concentration after 30min-2h, returns to baseline by 6-12h Highly specific, but falst negatives are common

Year 5 Path Immunology (6 decks)

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