5: Hypersensitivity Flashcards

1
Q

Types of hypersensitivity

A

Type :
I - IgE mediated, anaphylactic/immediate
II - antibody mediated
III - immune complex mediated
IV - delayed or T-cell mediated

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2
Q

In hypersensitivity reactions, the immune system

A

reacts in a way that damages the body rather than protecting it

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3
Q

Exaggerated immune reactions can lead to

A

Sepsis
Hypercytokinaemia (cytokine storm)
Organ dysfunction
Fatal tissue damage

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4
Q

Type I hypersensitivity

A

Mediated by IgE antibodies against environmental allergies
Immediate hypersensitivity - within mins
Targeted to multivalent environmental agents - allergens

Tested for by skin prick test - wheal and flare reaction to specific known allergens

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5
Q

Test for Type I hypersensitivity

A

Skin prick test, looking for wheal and flare reaction to specific allergens

two phases :
1. sensitisation phase
2. re-exposure leading to anaphylaxis

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6
Q

Sensitisation phase

A

Complex - mechanism not exactly understood, influenced by genetics, environment and age

Th2-cells and follicular Th cells produce IL-4 and IL-3
B cell class switching from IgM to IgE production
Th2 cells recruit eosinophils

IgE by B cells not found in circulation, loaded onto Fc receptors of mast cells and basophils

Allergen encountered again, cross-linking of two IgE bound on membrane of mast cell and basophils, leading to rapid immune reaction - sensitisation

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7
Q

Crosslinking causes

A

rapid degranulation, release of inflammatory mediators
- occurs at lower antigen concentrations than normal immune reactions

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8
Q

Phases of T1 hypersensitivity

A

3 phases :
Early phase- degranulation of mast cells, within minutes
Later response - within a few hours, recruitment of neutrophils
Late response - 3/4 days, eosinophils recruited, Th2 cells present

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9
Q

Anaphylaxis is a

A

medical emergency

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10
Q

Anaphylaxis can be treated by

A
  • adrenaline injection ; counteracting vasodilation, EpiPen
  • antihistamines
  • feet up to maintain brain perfusion
  • Monitor for biphasic anaphylaxis
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11
Q

Biphasic anaphylaxis

A

Unknown anaphylactic shock following first anaphylactic shock

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12
Q

Type II hypersensitivity

A

IgG or IgM mediated cytotoxicity reactions
Self-antibodies produced by self-reactive B cells (escaped tolerance)

Secrete self-reactive IgM or IgG when activated by self-reactive T cells

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13
Q

By which mechanisms can hypersensitivity II result in disease

A

Anti-receptor activity; blocking or activating its function
Antibody dependent cell-mediated cytotoxicity (ADCC)
Classical activation of complement cascade

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14
Q

Cytotoxic mechanisms of Type II hypersensitivity

A

Complement neutrophil activation
Membrane Attack Complex
Antibody opsonisation and phagocytosis
Natural Killer cells against antibodies

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15
Q

Receptor binding in Type II hypersensitivity

A

Blocking receptors e.g Myasthenia gravis
Activating receptors e.g. Graves’ disease

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16
Q

Type III hypersensitivity

A

Small soluble antigens make immune complexes less immunogenic, not removed by spleen
Self reactive B cells switched from IgM to IgG Production

immune complexes become deposited in blood vessel walls

17
Q

In type 3 hypersensitivity, immune complex deposition in blood vessel walls can lead to:

A

Activation of complement system
Activation of neutrophil degranulation
leads to tissue damage at site of deposition

18
Q

Example of Type 3 hypersensitivity

A

Systemic Lupus Erythematosus

19
Q

Systemic Lupus Erythematosus

A

Auto-antibodies against DNA and nuclear proteins
Complement activated by immune complexes, leading to :
damage by MAC formation
oedema by anaphylatoxins
neutrophil recruitment

20
Q

In Lupus (T3 hypersensitivity) immune complexes are deposited in

A

kidneys (blood filtration)
joints (synovial fluid, filtered from blood vessel walls)

21
Q

Compare Complement in Type 2 and Type 3 hypersensitivity

A

T2: Complement used in small amounts- because damage is localised
T3: Complement used in large amounts (C3 & C4 can be used as diagnostic markers)

22
Q

Compare Antigens in Type 2 and Type 3 hypersensitivity

A

T2: antigens cell-surface bound
self-antigens / foreign antigens e.g drugs

T3: antigens soluble
mostly self-antigens (except serum sickness)

23
Q

Compare damage in Type 2 and Type 3 hypersensitivity

A

T2: damage where immune complexes are formed (tissue specific)

T3: Damage where immune complexes are deposited (not tissue specific)

24
Q

Type IV hypersensitivity

A

T-cell mediated
Delayed-type hypersensitivity; T cell recruitment takes time
NOT antibody mediated
damage occurs through both CD4+ Th cell or CD8+ cytotoxic T cell

25
Reactions of type 4 hypersensitivity
Sensitisation phase Re-exposure and immune response
26
Use of T4 hypersensitivity in testing
Can be used in Mantoux skin test for TB (poison ivy)
27
Haptens
small proteins functioning as antigens when bound to proteins
28
Sensitisation phase of T4 hypersensitivity
Exposure leads to dendritic cell uptake DC present to specific naive T cells in lymph node T cells differentiate into mature Th1-cells --> form memory cells
29
Re-exposure in T4 hypersensitivity
Specific memory T cells respond, induce inflammation in tissue leads to Th1-cell expansion leads to Macrophage activation - incr. vascular permeability, causing swelling (oedema) and redness
30
Involvement of T cells in T4 hypersensitivity
Dependant on signals T cells receive from phagocytes - differentiation to Th17 cells; IL-17 secretion that recruits neutrophils -CD8+ self-specific cytotoxic T cells directly kill cells within antigens