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Immunology and Infection > Memory and Vaccination > Flashcards

Memory and Vaccination Flashcards

1
Q

what is immunological memory?

A
  • when infected for a second time get a much better response
  • B cells more specific
  • get lifelong immunity
  • vaccines stop the pathogen from being hyper aggressive
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2
Q

what is the response to the same pathogen?

A
  • secondary immune response
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3
Q

what is the secondary immune response governed by?

A

memory cells

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4
Q

what are the key features of memory cells?

A
  • faster
  • more powerful
  • more specific
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5
Q

what are the properties of memory T cells?

A
  • long lived small resting cells
  • numbers are consistent throughout our lives
  • express survival genes
  • requires the cytokine IL-7
  • high levels integrins
  • cytokine response faster and more powerful
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6
Q

what does the consistent numbers throughout life suggest about memory T cells?

A
  • a balance between proliferation and death
  • need a constant number
  • think they are stem cell like
  • memory cells spontaneously proliferating
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7
Q

what survival genes are expressed by memory T cells?

A
  • eg Bcl-2

- over expressing survival genes means a reduced ability to die off

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8
Q

why does the memory T cell require IL-7?

A
  • for survival
  • to memory cell for CD4 and CD8
  • memory cell CD8 also requires IL-15
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9
Q

what integrins are found on the surface of memory T cells?

A
  • LDA1 and CD2
  • helps them to respond/migrate quickly
  • makes a really strong immunological synapse
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10
Q

what are the properties of effector memory T cells?

A
  • CCR7 negative
  • rapidly matures into an effector cell
  • secrete large quantities of cytokines early after stimulation
  • express receptors for pro-inflammatory chemokines and integrins
  • specialised for rapidly entering inflammed tissue
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11
Q

what are effector memory T cells CCR7 negative?

A
  • secretes more cytokines than central memory T cell
  • put sentinels where the pathogen first came in
  • needs to make sure it resides in that one tissue
  • no CCR7 means its not responsive to CCL21/19 which draws T cells to lymph nodes
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12
Q

what are the properties of central memory T cells?

A
  • CCR7 positive
  • sentinels that circulate lymph node and spleen
  • take longer to be reactivated
  • do not secrete large amounts of cytokines
  • upon re-stimulation differentiate into effector memory T cells
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13
Q

what are the secondary response dominated by?

A
  • class switched B cells
  • in secondary exposure they have class switched IgG (compared to IgM)
  • more in tune and have a higher affinity
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14
Q

how long does it take to make B cell memory?

A
  • lag in making memory
  • slower to develop than memory T cells
  • at least * days to develop
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15
Q

why does it take B cells longer to make memory cells?

A

require CD4 helpter T cells and undergo somatic hyper mutation in the germinal centre

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16
Q

what is the role of FCyRIIB at the end of an immune response?

A
  • shits down signalling through BcR once pathogen is eradicated
  • signals to make sure only memory cells are triggered to respond during re-infection
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17
Q

how does FCyRIIB ensure only memory cells are active during re-infection?

A
  • expressed on B memory cells
  • antibodies that already exist can bind
  • bind pathogen molecule to naive B cell and signal through FCyRIIB to shut down B cells
  • only class switched antibodies produced
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18
Q

how does the CD4 T helper cell help the memory B cell?

A
  • BcR binds pathogne
  • higher levels of MHC II-peptide complexes and co-stimulatory molecules of memory B cells bind to CD4 T helper cells
  • CD4 T helper cell gives cytokine and co-stimulatory signals to the memory B cell to proliferate
  • move to the germincal centre and undergo somatic hyper mutation
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19
Q

what happens once the memory B cell is activated?

A
  • moves to germinal centre
  • somatic hyper mutation
  • leaves the lymph node
  • exists as long lived plasma cell in bone marrow or continues to recirculate
  • will still go through negative selection
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20
Q

what were the risks of virioliation?

A
  • viral load, aggressive infection leading to death
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21
Q

what was virioliation?

A

transmission of a small amount of the dangerous pathogen to induce a robust immune response upon secondary encounter

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22
Q

how did edward jenner develop vaccination to small pox?

A
  • use cowpox pus to infect someone which would protect them against smallpox
  • essentially took an attenuated version to elicit protective immunity
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23
Q

what is a vaccine?

A

a biologically prepared weakened version of a disease causing micro-organism that induces a robust immune response to the aggressive form of the microorganism upon secondary encounter

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24
Q

what is immunisation?

A

strategy to protect the host from disease

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25
Q

how can vaccination manipulate the immune system?

A
  • protect against disease causing pathogens
  • protect against or treat cancer
  • desensitise the immune system to allergens
  • desensitize auto-aggressive immune cells, or elecit regulatory T cell response, to control autoimmunity
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26
Q

what is the goal of vaccination?

A

to induce herd immunity

  • around 80% of the population needs to be immune for herd immunity to occur
  • takes away the reservoir for the pathogen to replication
27
Q

why is people not having vaccinations dangerous?

A
  • need to vaccinate a large number of the population in order to protect the population
  • vaccinated person could protect an unvaccinated person
28
Q

why does age predetermine a vaccine programme?

A
  • immune systems change over time
  • babies are susceptible as they do not have a fully formed immune system
  • as you get older the thymus shrinks
29
Q

what are the consequences of your thymus shrinking as you age?

A
  • make fewer new T cells
  • repertoire of T cells is reduced
  • when you’re older most circulating B and T are memory cells
  • may not have the T cells for a new pathogen
  • B cells need T cell help
30
Q

what can inducing neutralizing antibodies achieve?

A

blocks the pathogen from entering the cells and decreases damage to cells

31
Q

what do you need to consider when developing a vaccine?

A
  • how will you store it
  • how much will it cost
  • will you need boosters
32
Q

what two groups can immunisation be divided into?

A
  • passive

- active

33
Q

what is passive immunisation?

A
  • got a memory response, isolate the antibodies and give them to somebody who doesnt have protective immunity
  • can have natural or artificial passive immunity
34
Q

what is active immunisation?

A
  • give them a vaccine to make the immune system think its infected
  • can have natural or artificial active immunity
35
Q

what are some examples of natural passive immunisation?

A
  • natural via the placenta

- natural via colostrum (breast milk)

36
Q

what is the process of natural passive immunisation via the placenta?

A
  • foetus recieves maternal IgG
  • IgG is transported through endocytosis, can be very acific so binds to the molecule FcRn
  • when the pH rises IgG is released
  • transfer of IgG antibodies against toxins, viruses and bacteria
  • lasts around 3 months after birth
37
Q

what is the process of natural passive immunisation via the colostrum?

A
  • contains lysozyme, interferons and some leukocytes
  • high concentration of IgA
  • IgA results from stimulation of B cells in mothers intestine and migration to the breast
38
Q

what are some examples of artificial passive immunisation?

A
  • artificial and heterologous (different host), eg during WWI used anti-tetanus serum from horses
  • artificial and homologous (eg man to man), antibodies used for passive immunisation can be polyclonal or monoclonal
39
Q

how was using anti-tetanus serum from horses an example of artificial and heterologous passive immunisation?

A
  • protection was brief but powerful
  • horses have a good antibody response to tetanus toxin
  • take the serum and inject into the soldiers
40
Q

what were the main problems with using anti-tetanus serum from horses?

A
  1. catabolised and removed by the recipients immune mechanisms
  2. ‘serum sickness’; immune response to foreign antibody results in immune complex formation and depletion of complement
41
Q

what is polyclonal artificial passive immunisation?

A
  • taking plasma, get lots of antibodies and recognises lots of epitopes
  • multiple isotypes
  • multiple antigenic targets leads to diversity
42
Q

what is monoconal artificial passive immunisation?

A
  • single antibody isotype
  • single antigenic target
  • one BcR that is closed
43
Q

what is the process of artificial and homologous passive immunisation?

A
  • take serum from plasma from people who have protective immunity
  • can take the B cells that make the antibody
  • clone them and immortalise them
  • use in a vaccine
44
Q

what is active immunisation?

A
  • aims to achieve immunological

- give weakened versions of the pathogen to fool the immune system

45
Q

what was louis pasteurs discover?

A
  • found a weakened version of chicken cholera

- artifically induced damage to natural pathogen weakens the virulence of the pathogen yet induces excellent immunity

46
Q

what are the 3 I’s in active immunisation?

A
  • isolate
  • inactivate
  • inject
47
Q

what are live attenuated vaccines?

A
  • one dose to achieve a substantial immune response: body thinks its the real deal
  • get a B and T cell response
  • similar to natural infection
  • antigen processed and presented to CD4 and CD8 cells
  • will also lead to antibdoy production
48
Q

what is meant by attenuated?

A

altered pathogen does not cause disease but grows in host transiently

49
Q

how do you attenuate a pathogen?

A
  • grow in abnormal conditions
  • culture in an inappropriate host cell to induce mutations
  • put back into the human
  • wont infect but get an immune response
50
Q

what are the problems with a live attenuated vaccine?

A
  • can mutate back to wild-type pathogen in vaccinated host

- if its in the body for a long time - can’t give to immunocompromised people

51
Q

how do you genetically engineer an attenuated vaccine?

A
  • isolate and in vitro mutate the virulent gene
  • can generate mutants incapable of reversion to wild-type
  • idenfitiy parts that are receptor binding and core proteins
  • genetically manipulate the virus to reomve virulence
  • resulting virus is viable but avurilent
52
Q

what are the problems with killed/dead vaccines?

A
  • need several boosters to achieve a substantial immune response
  • good at producing an antibody response but not good for T cell response
  • inactivation must preserve the structure of immunogenic epitope
53
Q

what are the advantages of taking a reductionist approach to vaccination?

A
  • elicits an immune response only to desired antigens
  • less side effects
  • industrial production
54
Q

what are the disadvantages of taking a reductionist approach to vaccination?

A
  • requires detailed knowledge of the pathogen

- rarely immunogenic on their own - require adjuvants or viral vectors`

55
Q

what is the reductionist approach to vaccines?

A

too genetically synthesise the key components of the pathogen that induces a protective immune response

56
Q

why are polysaccharides poor at eliciting the correct type of B cell response which may be T cell dependent?

A
  • induce IgM antibodies but no memory
57
Q

how do we solve the problem of polysaccharides being poor at eliciting the correct type of B cell response which may be T cell dependent?

A
  • conjugate vaccines are constructed
  • bacterial polysaccharide chemically linked to T-dependent antigen tetanus toxoid protein
  • conjugate is internalised
  • tetanus toxin peptides induce T helper cells that secrete cytokines
  • cytokines act on the polysaccharide specfic B cells to class switch to an appropriate class of antibdoy
58
Q

how are polysaccharides used in the reductionist approach?

A

targets to make an immune response to as they will prevent the virus/bacteria entering the cell

59
Q

what are adjuvants?

A
  • components of killed or dead vaccines
  • materials used to boost the adaptive immune response
  • act on the innate immune response
  • complex that absorbs the vaccine, holds and stabilises it in your body
  • can tak multiple boosters
60
Q

what are the main types of action of adjuvants?

A
  1. act as a depot enhancing the time for APCs to find them
  2. stimulate innate immune cells to make the cells think they have seen a pathogen resulting in the release of cytokines
  3. transport the antigen to the lymph node
61
Q

why are viral vectors proving an effective way to carry pathogenic molecules into the immune system?

A
  • viral vector is relatively harmless, eliciting only mild-discomfort
  • boost a response to subunit vaccines
  • taking genes into adenovirus vector
62
Q

how are dendritic cell based vaccines gaining strength in cancer biology?

A
  • Tumour RNA is inserted into a dendritic cell  slight different from human cells
  • Transported into DC’s (modified)
  • The dendritic cell matures produces tumour antigens and is injected into patient and the dendritic cell displays tumour antigen and activates T cells
     Present tumour antigen to T cells
  • Activated T cells attack the cancer cell
     Try and destroy the tumour
63
Q

what are the key considerations when designing an effective vaccine?

A
  • balancing efficacy and safety
  • safety is always more important
  • cost stability and geography

Immunology and Infection (13 decks)

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