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Life Protection > Hypersensitivity > Flashcards

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
Q

Which cytokines are related from activated mast cells?

A
  • IL-3
  • IL-4
  • IL-13
  • TNFa

causes inflammation and an IgE switch

26
Q

How are mast cells involved in non-atopic allergy?

A

triggered by extreme temp and exercise

IgE and Th2 not involved

mast cells are hypersensitive to activation

20-30%: immediate hypersensitivity

27
Q

What is the late reaction in type 1 hypersensitivity?

A

occurs 2-24hr post initial reaction

appears without further allergen exposure

may last several days

common in allergic rhinitis, bronchial asthma

28
Q

What is the mechanism for the late reaction in type 1 hypersensitivity?

A

influx of:

  • eosinophils
  • neutrophils
  • basophils
  • Th2 cells

mediated by mast cell chemokines and cytokines
inflammation and damage to mucosal epithelia

Rx: corticosteroids

29
Q

What stain can be used to differentiate basophils and eosinophils?

A

= Wright-Giemsa staining

Basophil: purple granules

Eosinophil: red/brown granules

30
Q

How do eosinophils contribute to a type 1 hypersensitivity reaction?

A

Release of pre-formed mediators:
MBP
ECP
enzymes

Lipid mediators: leukotrienes

Cytokines:
IL-3, IL-5,
chemokines (IL-8, RANTES)

31
Q

What is anaphylaxis?

A

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
Q

How do type 2 and type 5 hypersensitivity responses differ?

A

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
Q

What are the mechanisms underlying type 2 hypersensitivity?

A
  • opsonisation and phagocytosis
  • complement activation and Fc receptor-mediated inflammation
  • Ab-mediated cellular dysfunction (no inflammation, no tissue damage)
34
Q

What are examples of conditions caused by type 2 hypersensitivity reactions?

A

autoimmune haemolytic anaemia
agranulocytosis
transfusion reactions
haemolytic disease of newborn

35
Q

What occurs in the complement-mediated reaction in type 2 hypersensitivity?

A
  • 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
Q

What causes Goodpasture’s syndrome?

A

type 2 hypersensitivity reaction

Ab directed against glomerular basement membrane

causes smooth, linear deposit

37
Q

What is the mechanism underlying antibody-mediated cellular dysfunction?

A

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
Q

What is the pathophysiology in myasthenia gravis?

A

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
Q

What are the mechanisms underlying a type 3 hypersensitivity reaction?

A

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
Q

What is serum sickness?

A

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
Q

What is SLE?

A

= systemic lupus erythematosus

type 3 hypersensitivity reaction

autoantibodies (often targeting nuclear Ag)

immune complexes deposit in tissues causing vasculitis

42
Q

How do the deposits in type 3 hypersensitivity reactions differ from that of type 2 hypersensitivity reactions?

A

Type 2: SMOOTH LINEAR deposit e.g. Goodpasture’s syndrome

Type 3: COARSE GRANULAR deposit
e.g. SLE

43
Q

What are the mechanisms underlying type 4 hypersensitivity reactions?

A

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
Q

What is the mechanism underlying DTH in type 4 hypersensitivity?

A

CD4+ Th1 cytokines (IFNg) cause inflammation

chronic macrophage activation lead to tissue injury

  • lysosomal enzymes
  • ROS, NO
  • inflammatory cytokine
45
Q

In Th1 response, what signals are required for macrophage activation?

A
  • TCR: MHCII-peptide complex
  • CD40L (Th1): CD40 (mQ)
  • IFNg secreted by Th1 cell
46
Q

What is the tuberculin reaction?

A

= 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
Q

What is the underlying cause of the tuberculin reaction seen in the Mantoux test?

A

= Perivascular accumulation of monocytes and CD4+ T cells

[DTH Type 4 reaction]hypersensitivity]

48
Q

What causes granulomatous inflammation in type 4 hypersensitivity reaction?

A
  • strong Th1 and macrophage activation -> tissue destruction
  • inflammatory cytokines (e.g. TNFa, IFNg)

e.g. in TB (persistent microbial inflammation)

49
Q

What is the cause of contact dermatitis?

A

= 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
Q

What are the causes of organ-specific and systemic autoimmune diseases?

A

= DTH type 4

Th1 cells: mQ infiltration

Th17 cells: neutrophil infiltration

  • RA
  • MS
  • IBD
  • Psoriasis
51
Q

What is cytotoxic T cell type 4 hypersensitivity?

A

= tissue destruction mediated by CTLs

e.g. T1DM, Hep B, transplant rejection

52
Q

What are the principles of Rx in hypersensitivity disorder?

A
  • avoid allergen or desensitisation

- reduce tissue injury

53
Q

What are e.g. of Rx that are used in hypersensitivity reactions?

A

[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
Q

Which immunosuppressive drugs may be used in hypersensitivity reactions?

A
  • cyclosporine (blocks T cell activation)
  • rapamycin
  • methotrexate (blocks lymphocyte proliferation)

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