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IMMUNOLOGY PART 1 DEN303 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Define hypersensitivity, give an example

A

Allergy or autoimmunity, e.g. asthma and allergic diseases (increasing in pop)

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2
Q

Why is hypersensitivity an issue in dentistry?

A

More people sensitive to latex, dental materials, drugs

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3
Q

What does acquired immunity consist of?

A 
Antibody response (humoral) and cell mediated response
= involved in hypersensitivity rxns
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4
Q

Features of antibody response?

A

Occurs quickly
Systemic or widespread
Bcos antibodies are soluble proteins that reach most parts of the body quickly by blood, tissue fluid and body secretions

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5
Q

What is cell mediated immunity directed against?

A

Tumour cells, virally transformed cells and foreign cells

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6
Q

What do cellular immune responses tend to be?

A

Localised, slow to develop and slow to resolve

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7
Q

How can the immune system fail?

Hypersensitivity = failure of immune system

A

Fail to produce adequate immune response - immunodeficiency

Produce an overactive, damaging response -hypersensitivity - allergy

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8
Q

What is hypersensitivity?

= failure of immune system

A

Immune system responds in exaggerated or inappropriate way = harm caused
Usually occurs on 2nd or subsequent exposure to antigen
Genetic susceptibility

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9
Q

Name the 4 types of hypersensitivity

A
  1. Immediate/anaphylaxis
  2. Cytotoxic
  3. Immune complex
    (1-3 = antibody mediated)
  4. Delayed = cell mediated
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10
Q

Features of immediate (1) hypersensitivity

A

Acute (anaphylaxis)
Rapid onset
IgE mediated

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11
Q

How does immediate hypersensitivity work?

A
  1. Allergen exposure
  2. T cells bind to allergen (Antigen presenting cell)
  3. T cell differentiates into Th2
  4. Th2 = antibody production, release IL4
  5. High IL4 = increase IgE from plasma cell = more humoral response
  6. Mast cells and basophils express FcE receptors and contain histamine granules
  7. IgE in plasma bind to receptors on mast cells
  8. = Sensitisation = IgE produced
  9. 2nd exposure to allergen
  10. Clusters form and mast cells degranulate and secret IL5
  11. Eosinophils attracted = mass cell release of histamine
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12
Q

Who is susceptible to type 1 hypersensitivity? What is an allergen?

A

High IgE levels

Allergen = Ag that gives rise to type 1 hypersensitivity - most are small proteins e.g. pollen - grass

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13
Q

Cellular response of type 1?

A

Mast cell and basophils expressed FcE receptors and contain histamine granules
IgE in plasma binds to receptors
Allergen exposure
Sensitisation = IgE prodcued
2nd exposure to allergen = IgE binds to allergen
Clusters form and mast cell degranulates and secretes IL-5 = attracts eosinophils = mass release of histamine

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14
Q

What does histamine release cause?

A 
Vascular dilation
Increase vascular permeability e.g. oedema
Bronchospasm
Urticarial rash
Increase nasal and lacrimal secretions
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15
Q

What does type 1 hypersensitivity most commonly present as?

A

Hay fever, asthma, acute allergic response - angio-oedema/anaphylaxis

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16
Q

Diagnosis - wheel and flare skin test?

A

Apply allergen under skin using prick test - response within 5 mins
Wheel caused by extravasation of serum into skin due to histamine - angio-oedema
Flare (red patch) due to axon reflex
Late phase (6hrs plus) due to leukocyte infiltrate and more oedema

17
Q

How to manage type 1 hypersensitivity?

A

Adrenaline, antihistamines, corticosteroids, avoidance of allergen

18
Q

Features of type 2 hypersensitivity

A

Antibody mediated - antibodies target cell surface self antigens (auto-antibodies)

  • Usually IgG or IgM
  • Antibodies induce: cell damage, inflam
19
Q

Type 2 - what do autoantibodies activate?

What are type 2 rxns important in?

A

ADCC, complement

Important in:
- Acute transplant rejection / blood transfusion
- Haemolytic Disease of the Newborn
- Autoimmune diseases e.g. Pemphigus
„ Pemphigoid
20
Q

What does complement and ADCC activation in type 2 result in?

A

Inflammation and cell death (by membrane attack complex)

ADCC = inflam, cell death

21
Q

Haemolytic disease of newborn - type 2 hypersensitivity?

A
  1. First Pregnancy - RhD+ baby’s blood enters RhD- mother’s circulation
  2. Baby born BUT mother
    raises Ab to RhD
  3. Second Pregnancy – If
    foetus is RhD+ mother
    IgG crosses placenta and
    will destroy foetal
    erythrocytes
  4. SO – preformed anti-RhD Ab given to Rh- mothers after delivery of RDH+ infants
22
Q

What is pemphigus? (type 2)

A

Auto-antibodies against desmoglein-1 and 3
Ab prevents formation of gap junctions between epithelial cells
Epithelial shedding - mainly mucosal

23
Q

What is pemphigoid? (type 2)

A

Auto-antibodies against hemidesmosomes
Ab prevents binding of epi with dermis at basement membrane
Epi shedding - skin and mucosal

24
Q

Type 3 hypersensitivity?

A

Immune complex - mediated hypersensitivity
Immune complexes form between antigen and antibodies
These complexes form in the serum
Diff to type 2 which are cell based

25
Q

Type 3 - where may immune complexes deposit in?

A

Lining of BV, glomeruli, lung

26
Q

Type 3 - what do the immune complexes induce in the BV lining, glomeruli and lung?

A

Complement activation, leukocyte binding and inflam at localised site

27
Q

How does vascular permeability increase in type 3?

A
  1. Immune complexes normally bind C’ = binds to CR1 on erythrocytes which are removed in liver
  2. In inflammation, immune
    complexes bind to blood vessels where they act on platelets and basophils
  3. These are then activated and release vasoactive peptides
    (histamine)
  4. This increases vascular
    permeability
28
Q

What does an increased vascular permeability allow? - Type 3

A
  1. More immune complexes to be deposited
  2. Induced platelet aggregation and C’ activation
  3. Neutrophil attracted but cannot ingest complexes
  4. = Secrete lysosomal enzymes = further tissue damage
29
Q

What is immune complex mediated hypersensitivity important in? - type 3

A

Immune complex mediated vasculitis e.g. erythema multiforme, SLE
Treatment - immunosuppression with steroids

30
Q

What is erythema multiforme? - type 3

A

Skin condition mediated by deposition of immune complex in the superficial microvasculature of the skin and oral mucous membrane - usually follows infec/drug exposure

31
Q

What is type 4 hypersensitivity?

A

Cell mediated immunity/delayed type hypersensitivity
T cell mediated
Slow to develop (12-48hrs), resolve and is localised

32
Q

How does type 4 hypersensitivity occur?

A

T cell recognises antigen expressed on another cell in the context of MHC
T cell can respond by;
- Releasing cytokines (by CD4+)
- Killing the target cell (by CD8+)

33
Q

What are cell mediated immune responses important in? - type 4

A

Delayed type hypersensitivty responses
Contact hypersensitivty - dermatitis
Lichenoid reactions to amalgam fillings and other materials

34
Q

How does contact dermatitis - type 4 occur?

A

Sensitisation;

  1. Ag gets into skin and is internalised by langerhans cells = special ACP in the epidermis
  2. These travel to lymph nodes and present Ag to CD4+ cells
  3. These form memory CD4+ cells
35
Q

How does type 4 hypersensitivity occur? When is tissue damage seen and resolved?

A
  1. Langerhans cells move from epidermis to dermis
  2. They present Ag to memory CD4+ T cells
  3. These are activated and
    secrete IFNγ.
  4. This increases expression of ICAM-1 and MHCII on Keratinocytes
  5. And causes secretion of proinflammatory cytokines
  6. More leukocytes are
    attracted to site
  7. Neutrophils arrive after 4 h,
    monocytes and T cells after 12h & secrete tissue damaging cytokines

-Tissue damage seen at post
12h (delayed)
- Tissue damage resolve if Ag removed

36
Q

How to test for type 4?

A

Skin patch testing - samples applied to skin of back or arm for 72-96 hrs

37
Q

Lichenoid rxn to amalgam?

A

Type 4 contact hypersensitivity response to mercury or amalgam
Positive skin path test response to mercury or amalgam
Lesion resolves on removing the filling

IMMUNOLOGY PART 1 DEN303 (5 decks)

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