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Hypersensitivity Flashcards

1
Q

What classification system categorises hypersensitivity reactions?

A

Gell and Combs
4 main types
type 5 recently added

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2
Q

What is a type 1 hypersensitivity reaction?

A

anaphylaxis
caused by Ag reacting with IgE bound mast cells
other e.g. include atopy (asthma, hay fever, allergy)

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3
Q

What is a type 2 hypersensitivity reaction?

A 
cell bound 
caused by IgG or IgM binds to antigen on cell surface
e.g. Autoimmune haemolytic anaemia
• Idiopathic Thrombocytopenic Purpura
• Goodpasture's syndrome
• Pernicious anaemia
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4
Q

What is a type 3 hypersensitivity reaction?

A 
immune complex
caused by free antigen and antibody (IgG, IgA) combining
e.g. Serum sickness
• Systemic lupus erythematosus
• Post-streptococcal glomerulonephritis
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5
Q

What is a type 4 hypersensitivity reaction?

A 
delayed hypersensitivity 
T cell mediated
e.g. • Tuberculosis
• Graft versus host disease
• Allergic contact dermatitis
• Scabies
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6
Q

What is a type 5 hypersensitivity reaction?

A

Autoantibodies
Antibodies that recognise and bind to the cell surface receptors.

This either stimulating them or blocking ligand binding

e.g. Graves disease, myasthenia graves

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7
Q

What is hypersensitivity?

A

diseases caused by abnormal immune responses, which then cause tissue damage

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8
Q

What are the characteristics of hypersensitivity reactions?

A
  • triggered by environmental or endogenous Ag
  • imbalance of effector mechanisms and regulatory/control mechanisms
  • genetic predisposition
  • tissue injury mediated through same immune cascades used to treat infection
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9
Q

What are the mechanisms underlying ‘Ab binding?’

A
  • complement activation => inflammation
  • FcR activation => inflammation
  • stimulating/blocking Ab
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10
Q

What is the main T cell mediated mechanism for hypersensitivity?

A

delayed type hypersensitivity, cell lysis

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11
Q

What is the nature of a type 1 hypersensitivity reaction?

A

fast immune reaction to sensitised subject

triggered by expo to allergens

allergen binds to IgE on mast cell surface

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12
Q

What is atopy?

A

increased propensity to develop allergies

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13
Q

What are the risk loci implicated in type 1 hypersensitivity responses?

A

Chr 5q31

locus which encodes genes for IL-4, IL-5, IL-13: Th2 responses

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14
Q

What environmental factors may increase risk for development of Type 1 hypersensitivity reactions?

A
  • pollutants
  • respiratory infections
  • bacterial skin infections
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15
Q

What is the hygiene hypothesis?

A

increased allergy incidence in developed countries

related to reduced infections in early life

childhood infections educate immune system so it is less likely to react to innocuous allergens

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16
Q

What is the mechanism underling type 1 hypersensitivity?

A
  • DC present Ag to CD4+ T cells
  • Th2 cell response
  • B cell activation and IgE switch
  • IgE production
  • IgE bind Fc receptors on mast cells (sensitisation)
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17
Q

Where are mast cells located?

A
  • located to small vessels e.g. capillaries
    in tissue depots

mature upon tissue entry

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18
Q

What are the main stages in the allergen exposure in type 1 hypersensitivity?

A
  • allergen crosslinks IgE-FcR on mast cells
  • mast cell activation
  • inflammatory mediator release
  • vascular/smooth muscle reactions [mins]
  • LATE phase reaction [2-24hr]
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19
Q

Which cells carry the IgE-FcR?

A

FcR = epsilon receptor for IgE

  • mast cells
  • eosinophils
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20
Q

What Rx suppresses the expression of pro-inflammatory cytokines?

A

corticosteroids

promoter function is repressed

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21
Q

What is the relationship between mast cell degranulation and allergic response?

A

the more mast cells that degranulate over a wide body system/SA, the more widespread/systemic the reaction is

local response vs anaphylaxis

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22
Q

What happens when mast cells are activated?

A
  • release of preformed mediators
  • secretion of lipid mediators
  • release of cytokines
23
Q

Which preformed mediators are released by activated mast cells?

A
  • histamine

- enzymes

24
Q

Which lipid mediators are released from activated mast cells?

A
  • PGs
  • leukotrianes
  • platelet activating factor
25
Which cytokines are related from activated mast cells?
- IL-3 - IL-4 - IL-13 - TNFa causes inflammation and an IgE switch
26
How are mast cells involved in non-atopic allergy?
triggered by extreme temp and exercise IgE and Th2 not involved mast cells are hypersensitive to activation 20-30%: immediate hypersensitivity
27
What is the late reaction in type 1 hypersensitivity?
occurs 2-24hr post initial reaction appears without further allergen exposure may last several days common in allergic rhinitis, bronchial asthma
28
What is the mechanism for the late reaction in type 1 hypersensitivity?
influx of: - eosinophils - neutrophils - basophils - Th2 cells mediated by mast cell chemokines and cytokines inflammation and damage to mucosal epithelia Rx: corticosteroids
29
What stain can be used to differentiate basophils and eosinophils?
= Wright-Giemsa staining Basophil: purple granules Eosinophil: red/brown granules
30
How do eosinophils contribute to a type 1 hypersensitivity reaction?
Release of pre-formed mediators: MBP ECP enzymes Lipid mediators: leukotrienes Cytokines: IL-3, IL-5, chemokines (IL-8, RANTES)
31
What is anaphylaxis?
systemic type 1 hypersensitivity reaction Activation of mast cells in many tissues Sx: vascular shock, hypotension, airway and systemic oedema, vomiting, abdo cramps, diarrhoea
32
How do type 2 and type 5 hypersensitivity responses differ?
type s: autoantibodies directed against self Ag on host surface type 5: autoantibodies are directed against host PM receptors e.g. Graves, myasthenia gravis
33
What are the mechanisms underlying type 2 hypersensitivity?
- opsonisation and phagocytosis - complement activation and Fc receptor-mediated inflammation - Ab-mediated cellular dysfunction (no inflammation, no tissue damage)
34
What are examples of conditions caused by type 2 hypersensitivity reactions?
autoimmune haemolytic anaemia agranulocytosis transfusion reactions haemolytic disease of newborn
35
What occurs in the complement-mediated reaction in type 2 hypersensitivity?
- Ab deposit in tissues - complement activation -> inflammation - neutrophil recruitment, monocytes - leukocyte activation (Fc and complement receptors) - tissue damage e.g. Ab-mediated glomerulonephritis, vascular rejection
36
What causes Goodpasture's syndrome?
type 2 hypersensitivity reaction Ab directed against glomerular basement membrane causes smooth, linear deposit
37
What is the mechanism underlying antibody-mediated cellular dysfunction?
Ab bind to cellular receptors/proteins this MODIFIES FUNCTION e.g. myasthenia gravis: blocking Ab Graves disease: stimulating Ab NO INFLAMMATION, NO TISSUE DAMAGE
38
What is the pathophysiology in myasthenia gravis?
Ab bind and block the Ach receptors on the post-synaptic membrane preventing Ach to bind at activate them this causes severe muscle weakness
39
What are the mechanisms underlying a type 3 hypersensitivity reaction?
self/foreign antigen or soluble antigen Ab combine with Ag in circulation (IMMUNE COMPLEX) deposition of immune complex in vessel walls Causes systemic effects: glomerulonephritis, arthritis, vasculitis
40
What is serum sickness?
type 3 hypersensitivity caused by diphtheria immunisation, horse serum Immune complexes formed in circulation deposit in small arteries, glomeruli and synovia inflammation caused by complement activation injury caused by neutrophil influx
41
What is SLE?
= systemic lupus erythematosus type 3 hypersensitivity reaction autoantibodies (often targeting nuclear Ag) immune complexes deposit in tissues causing vasculitis
42
How do the deposits in type 3 hypersensitivity reactions differ from that of type 2 hypersensitivity reactions?
Type 2: SMOOTH LINEAR deposit e.g. Goodpasture's syndrome Type 3: COARSE GRANULAR deposit e.g. SLE
43
What are the mechanisms underlying type 4 hypersensitivity reactions?
mediated by either CD4+ or CD8+ T cells ``` CD4+: delayed hypersensitivity (e.g. TB), Th1 and Th17-mediated autoimmune disease ``` CD8+: type 1 DM, viral hepatitis-mediated cirrhosis, organ transplant rejection
44
What is the mechanism underlying DTH in type 4 hypersensitivity?
CD4+ Th1 cytokines (IFNg) cause inflammation chronic macrophage activation lead to tissue injury - lysosomal enzymes - ROS, NO - inflammatory cytokine
45
In Th1 response, what signals are required for macrophage activation?
- TCR: MHCII-peptide complex - CD40L (Th1): CD40 (mQ) - IFNg secreted by Th1 cell
46
What is the tuberculin reaction?
= DTH type 4 hypersensitivity in previously 'sensitised' individual (TB, BCG vaccination) Ag administered intradermally Checked at 72hr Ag is purified protein derivative (PPD) ``` 24-72hr later: erythema, oedema (8-12h) - accumulation of monocytes, CD4+ T cells - ROS, NO - inflammatory cytokines ```
47
What is the underlying cause of the tuberculin reaction seen in the Mantoux test?
= Perivascular accumulation of monocytes and CD4+ T cells [DTH Type 4 reaction]hypersensitivity]
48
What causes granulomatous inflammation in type 4 hypersensitivity reaction?
- strong Th1 and macrophage activation -> tissue destruction - inflammatory cytokines (e.g. TNFa, IFNg) e.g. in TB (persistent microbial inflammation)
49
What is the cause of contact dermatitis?
= DTH type 4 local expo to chemicals/allergens e.g. nickel, poison ivy protein conjugates are taken up by DC cells -> Th1 cells T cell and mQ infiltration shows as VESICULAR dermatitis
50
What are the causes of organ-specific and systemic autoimmune diseases?
= DTH type 4 Th1 cells: mQ infiltration Th17 cells: neutrophil infiltration - RA - MS - IBD - Psoriasis
51
What is cytotoxic T cell type 4 hypersensitivity?
= tissue destruction mediated by CTLs e.g. T1DM, Hep B, transplant rejection
52
What are the principles of Rx in hypersensitivity disorder?
- avoid allergen or desensitisation | - reduce tissue injury
53
What are e.g. of Rx that are used in hypersensitivity reactions?
[reduces tissue injury] Plasmapharesis: remove circulating Ab or immune complexes that can cause hypersensitivity reactions OMALIZUMAB: block IgE effects SODIUM CROMOGLYCATE: block mast cell degranulation HISTAMINE H1R ANTAGONISTS CORTICOSTEROIDS mAb INFLAMMATORY CYTOKINES (anti-TNF, IL-1 antagonist) ANTI-INTEGRIN Ab: block T cell entry into tissues
54
Which immunosuppressive drugs may be used in hypersensitivity reactions?
- cyclosporine (blocks T cell activation) - rapamycin - methotrexate (blocks lymphocyte proliferation)

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