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Cellular basis of immunity > Adjuvants > Flashcards

Adjuvants Flashcards

1
Q

Main types of vaccines

A

live, killed, sub-unit and naked dna

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2
Q

many vaccines developed now just contain specific elements

A

subunit vaccines contain individual proteins or polysaccharides- which evokes an immune response

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3
Q

what is an adjuvant

A

a substance that is formulated as part of a vaccine to enhance its ability to induce protection against infection

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4
Q

the word adjuvant comes from the latin meaning

A

to help

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5
Q

adjuvants help to activate the immune system..

A

allowing the antigens in the vaccine to induce long-term protective immunity

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6
Q

an effective vaccine will

A

stimulate both arms of the immune system- innate and adaptive

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7
Q

when does innate immunity start

A

within hours

- the adaptive developed several days later and involves coordination and expansion of immune cells called T and B cells

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8
Q

adaptive memory including b and t cells leads to

A

adaptive memory

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9
Q

why are adjuvant important

A

the whole point of a vaccine is to provoke immune memory, this makes sure the adaptive immune system is suitably stimulated

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10
Q

summary of importance of adjuvants

A

important for activating the innate immune response, resulting in improved adaptive immunity with enhanced activation of T and B cells

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11
Q

why ar they needed

A
  • to increase magnitude of response
  • to increase the duration of protective immunity
  • may allow the type of immune response to be modified
  • allow lower dose of vaccine to be used
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12
Q

types of adjuvant

A 
depot
delivery vehicles
immune stimulators (modifiers)
  • often adjuvants will have a combination of these properties
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13
Q

main activities of adjuvants

A

1) sustain release of antigen at site of injection 9depot)
2) up regulation of cytokines and chemokine
3) cellular recruitment at the site of injection
4) increase antigen uptake and presentation to APCs
5) activation and maturation of APC (increases MJHC II expressing and co-stimualtory molecules) and migration to the lymph nodes
6) activation of inflammation

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14
Q

depot effect

A

sustained released of antigen at site of injection

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15
Q

depot effect explained

A
  • antigen is sequestered at the site of injection and released over time
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16
Q

benefit of depot

A

exposes immune system to antigen for prolonged period of time
- means constant stimulation off immune system for production of high antibody titres

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17
Q

two ways in which adjuvants are delivered

A

Entrapped in a physical strictures that break down slowly-in liposomes

Entrapped in a matrix that dissociates slowly- Al+ salts

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18
Q

Lipsosomes

A

double phospholipid bilayer- encapsulates the antigens and breaks down slowly- depot effect

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19
Q

Aluminium salt

A

trap antigens in a matrix that dissociated slowly

- most widely used

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20
Q

adjuvant antigens are targeted to

A

APCs

  • bacterial proteins are processed by APCs
  • -> to trigger CD4/8 responses- cytotoxic and antibodies
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21
Q

Vaccines attach dot articles can be taken up by APCs and

A

enter the MHC II pathway to stimulate CD4 response- helper T cell

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22
Q

lipsoosme delivery means that antigens enter the

A

cytosolic pathway- stimulation of CD8 T cells- cytoxicity

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23
Q

lipsosmal carriers..

A

fuse with the membrane of APCs

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24
Q

how do cytokines, chemokine and tnerferons shape the immune response

A

bacterial proteins (vaccines) ar reprocessed by APCs

  • Toll agonists activate APCs like dendritic cells to present antigens
  • cytokines produced activated CD4+ AND CD8+
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25
Q

cytokines of CD8+

A

IFNgamma, IL-2, cytolytic capacity

26
Q

CD4+ T cell cytokines

A

Th1 phenotype, IFNgamma, IL-2, MIP1a

27
Q

what diggers immature DC to become mature DC

A

when TLRs present their antigens to T cells

28
Q

examples of molecules recognised by innate immune system

A

cell wall components, nucleic acid, conserved surface proteins, conserved stress proteins

29
Q

TLR signalling and inflammatory responses - process

A

1) recognition of bacterial molecule by TLR
2) dimerisation of TLR
3) signalling and inflammatory responses
4) important to produce enough cytokines to trigger adaptive immune system

30
Q

Two pathways of TLR signalling

A

My`d88 and TRIF

31
Q

MyD88

A 
inflammatory genes
- cytokines
-chemokines
endothelial adhesion molecules
- co-stimualotry molecules
32
Q

MyD88 causes

A

acute inflammation and stimulation of adaptive immune system

33
Q

TRIF

A
  • expression of type 1 interferon (IFN) genes
  • secretion of the 1 IFN
  • antiviral state
34
Q

example of TLR agonist

35
Q

example of a TLR agonist which are potents adjuvants

36
Q

why ar eLPS potent adjuvants

A
  • activate MyD88 and TRIF

- production of cytokines, chemokine, interferons, shaping the adaptive immune response

37
Q

LPS is a key component of

A

gram neg bacteria

38
Q

which TLR recognises LPS

39
Q

binding of LPS to TLR4 to causes MyD88 and TRIF response

A

1) cannot bids directly
2) therefore bids to the TLR4-MD-2 complex
3) lipid A pof LPS is bound by MD-2
4) causes dimerisation of TLR4
5) which triggers both MyD88 pathway and TRIF

40
Q

which part of LPS trigger TLR

A

the sugars

41
Q

dangers of modifier adjuvants

A

over activation of the immune system during infectious disease leads to cytokine stop- sepsis- where positive feedback loop is out of control

42
Q

what causes most spesis

43
Q

toxicity is a consequence of TLR pathway activation which produces

A

IL1, IL6, TNFa,- key mediators

44
Q

adjuvants vs toxicity

A

must be a balance of adjuvant effects of LPS and the possibility of over stimulation- sepsis
–> hard to gage amount of LPS

45
Q

LPS cannot be used directly as an adjuvant because

A

hard to age amount needed

46
Q

how can be LPS be used

A

when LPS Lipid A is modified

47
Q

what anchors LPS into the membrane

48
Q

how is LPS lipid A modified

A

a single phosphate is removed (there are two in total)- to generate Monophosphoryl Lipid A (MPLA)

49
Q

Monophosphoryl Lipid A (MPLA)

A

is non -toxic, however a weaker adjuvant, reaching risk of cytokine storm

50
Q

difference between LPS and MPLA

A

MPLA has one of LPS phosphates removed

51
Q

MPLA and MyD88

A

weaker reaction than LPS has

52
Q

MPLA and TRIF

A

both MPLA and LPS have good activation

53
Q

summary of difference in activation of TKR pathways

A

both pathways are activated by LPS- only TRIF pathway is significantly activated with MPLA

54
Q

how does MPLA reduce risk of sepsis

A

due to MyD88 not being significantly activated, a different repertoire of cytokines are produced

  • reducing risk of slide effect
  • therefore MPLA is now used as a vaccine adjuvant§
55
Q

why don’t live and killed vaccines require adjuvants

A

snelf-adjuvating

  • have peptidoglycan and LPS
  • increased cell signalling
56
Q

why are live and killed cells self-adjuvating

A
  • whole cells have agonist son TLR

- they can get information to the cytosol and trigger MHCI/II

57
Q

why are lived and killed not so popular if they are self adjuvating

A

due to risk of side effects- combination of many responses

58
Q

do adjuvants cause side effects of vaccines?x

A

its hard to say- not certain

- lots are now based on aluminium salts- neurodegenerative diseases e.g. narcolepsy with bird flue vaccines

59
Q

adjuvants are essential for almost

A

all modern vaccines

60
Q

adjuvants acts as

A

depots, delivery ebjicles or by activating TKR pathways (often combo)

Cellular basis of immunity (59 decks)

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