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respiratory lectures > hypersensitivity and the lung > Flashcards

hypersensitivity and the lung Flashcards

1
Q

what are hypersensitivity reactions

A

an overreaction of the immune system to an antigen which would not normally trigger an immune response

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2
Q

what does unwanted activation of the immune system do

A

leads to healthy tissue damage

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3
Q

what are self antigens

A

antigens produced by the organism’s own body cells

the immune system does not recognise as foreign antigens

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4
Q

impact of genetics on hypersensitivity

A

overreaction to unharmful antigens - linked to changes in CD regions of T helper cells

overreaction to self antigens - normally due to failure in central tolerance - this can have genetic features

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5
Q

what happens to an antigen the first time it enters the body

A
  1. picked up by antigen-presenting cells - eg as macrophages or dendritic cells
  2. taken to the nearest lymph node, where it is presented to naïve T-cells.
  3. cross-linking of the antigen with T-cells, as well as co-stimulatory molecules, can lead to activation of that T-cell and subsequent differentiation into “primed” Th1, Th2, or Th17 cells, which are specific to that antigen
  4. these can stimulate further immune responses if they meet the antigen again
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6
Q

what happens if T cells meet the same antigen again

A

can result in a hypersensitivity reaction

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7
Q

what is Coombs and Gell classification

A

divides hypersensitivity reactions into 4 types
1. immediate (type I)
2. cytotoxic (type II)
3. immune complex-mediated (type III),
4. delayed hypersensitivity (type IV) reactions

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8
Q

what induces mast cell activation in type 1 reactions

A

secretion of IgE antibodies

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9
Q

what does initial exposure to the antigen cause in type 1 reactions

A
  1. the priming of Th2 cells & their release of IL-4 causes the B cells to switch their production of IgM to IgE antibodies which are antigen-specific.
  2. the IgE antibodies bind to mast cells and basophils, sensitising them to the antigen
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10
Q

what happens when the antigen enters the body again in type 1 reactions

A
  1. it cross links the IgE bound to the sensitised cells, causing the release of preformed mediators including histamine, leukotrienes and prostaglandins
  2. this leads to widespread vasodilation, bronchoconstriction, and increased permeability of vascular endothelium
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11
Q

how can you divide the type 1 reaction into 2 parts

A

1: immediate - when release of pre-formed mediators causes the immune response

2: late phase response - 8-12 hours later, where cytokines released in the immediate stage activate basophils, eosinophils, and neutrophils even though the antigen is no longer present

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12
Q

what is anaphylaxis

A
  • systemic response to an antigen
  • leads to bronchoconstriction and vasodilation
  • causes decline in oxygen transportation
  • leads to anaphylactic shock and possibly death
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13
Q

how to treat anaphylaxis

A
  1. adrenaline - to dilate the bronchioles and constrict the blood vessels
  2. antihistamines - to reduce the inflammatory effects of histamine
  3. corticosteroids - to reduce systemic inflammation.
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14
Q

what mediates type 2 reactions

A

antibodies targeting antigens on cell surfaces

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15
Q

what begins the immune response in type 2 reactions

A

when cell surface antigens are presented to T cells

the cells which antigens are attached to are targeted

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16
Q

what happens when antibodies bind to cells in type 2 reactions

A
  • can activate the complement system
    leads to :
    • degranulation of neutrophils
    • a release of oxygen radicals
    • eventual formation of membrane
      attack complex
      these all lead to cell destruction

parts of the complement activation can also opsonise the target cell, marking it for phagocytosis

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17
Q

what does destruction of host cells lead to

A

tissue specific damage

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18
Q

what causes type 2 hypersensitivity reactions

A

in response to host cells - eg autoimmune
or
to non-self cell - eg blood transfusion reactions.

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19
Q

how are type 2 reactions distinguished from type 3

A

type 2 - antigens are cell bound

type 3 the antigens are soluble

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20
Q

what are acute transfusion reactions

A

when an inappropriate blood transfusion is administered and a patient is given blood not matching their ABO type

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21
Q

what do acute transfusion reactions lead to

A

activation of complement and widespread haemolysis by tumour necrosis factor and other interleukins,

  • can be fatal
22
Q

what mediates type 3 hypersensitivity reactions

A

antigen-antibody complexes in the circulation that may be deposited in and damage tissues

23
Q

what kind of tissues are antigen-antibody complexes lodged in in type 3 reactions

A

the complexes may become lodged in the basement membranes of tissues which have particularly high rates of blood filtration - eg the kidney and synovial joints

24
Q

what happens once the antigen-antibody complexes have become lodged in type 3 reactions

A
  1. the immune complexes rapidly and significantly activate the complement chain
  2. causing local inflammation and attraction of leucocytes
  3. results in:
    - increased vasopermeability
    - the attraction and degranulation of neutrophils
    - the release of oxygen free radicals which can severely damage surrounding cells.
25
Q

what is rheumatoid arthirits

A

can occur when antigen-antibody complexes circulate in the bloodstream end up lodging in the complex filtration systems responsible for maintaining the levels of synovial fluids at synovial joints

26
Q

what does rheumatoid arthritis lead to

A

the lodged immune complexes can cause a local inflammatory response, leading to stiffness and pain in affected joints

27
Q

what are type 4 hypersensitivity reactions mediated by

A

antigen-specific activated T-cells.

28
Q

what happens to the antigen when it enters the body in type 4 reactions

A

it is processed by antigen-presenting cells and presented together with the MHC II to a Th1 cell

29
Q

what happens if the T-helper cell has already been primed to that specific antigen in type 4 reactions

A
  • it will become activated.
  • then releases chemokines to recruit macrophages and cytokines such as interferon-γ to activate them
30
Q

what do activated macrophages do in type 4 reactions

A
  • release pro-inflammatory factors
    leading to local swelling, oedema,
    warmth, and redness
  • secrete lysosomal elements and reactive oxygen species
    leading to local tissue damage
31
Q

what is cell-mediated toxicity

A

when CD8+ T cells are involved in type 4 reactions

a foreign antigen is detected on a cell, eg in organ rejection

results in recruitment and activation of macrophages

32
Q

why is type 4 hypersensitivity reaction also known as delayed-type hypersensitivity

A

has a longer time period to appear following antigen exposure.

takes longer than all other types because of the length of time required to recruit cells to the site of exposure – around 24 to 72 hours.

33
Q

what is the reactant in type 1 reactions

A

IgE

34
Q

what is the reactant in type 2 reactions

A

IgG

35
Q

what is the reactant in type 3 reactions

A

IgG

36
Q

what is the reactant in type 4 reactions

A

T effector cells

37
Q

summary of type 1 reaction mechanism

A

mast-cell activation releases histamines and other mediators

38
Q

summary of type 2 reaction mechanism

A

antigens embedded in host cells cause complement activation and destruction by MAC

39
Q

summary of type 3 reaction mechanism

A

antibody binds to soluble antigen, forming a circulating immune complex lodges in a vessel wall and causes a local inflammatory response. APC activates Th1/CTL. T cells activation macrophages and cause an inflammatory response.

40
Q

summary of type 4 reaction mechanism

A

APC activates Th1/CTL. T cells activation macrophages and cause an inflammatory response

41
Q

example of type 1 reaction

A

Anaphylaxis

42
Q

how long do type 1 reactions take

A

minutes

43
Q

how long do type 4 reactions take

A

days

44
Q

example of type 2 reaction

A

Acute Transfusion Reaction

45
Q

examples of type 3 reactions

A
  • Rheumatoid Arthritis
  • Vasculitis
  • Glomerulonephritis
46
Q

examples of type 4 reactions

A
  • Contact Dermatitis
  • Mantoux tuberculin test
47
Q

when are IgM antibodies made

A

at the beginning of infection

48
Q

what are IgG antibodies

A

highly specific molecules targeting single ‘epitopes’

49
Q

when are IgE antibodies made

A

in response to things we’re allergic to

50
Q

which cells produce antibodies

A

B - lymphocytes

respiratory lectures (15 decks)

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