Lecture 15-Immunological memory and vaccination Flashcards

1
Q

Describe protective immunity?

A

Once you have an infection, you get the initial adaptive immune response. Then have a period where the antibody levels and t cells stay at a level where they can immediately protect body.
Then the effector cells gradually fall off.
(Then have memory compartment that survives for long time.)

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2
Q

Features of immunological memory?

A

Primary adaptive response to infection= slow and weak
Secondary exposure to same pathogen-> greater response

Secondary exposure is more rapid, better-> best affinity

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3
Q

Describe which Immunoglobulins are present in primary and secondary response?

A

Primary- IgM most prominent, then some IgG.

Secondary- a bit of IgM and loads of IgG
IgG has higher affinity than IgM

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4
Q

What are the changes to the immune cells associated with memory?

A
  1. Expansion of “clones” of cells with re-arranged antigen receptor genes specific for the primary antigen encountered (TCRs and BCRs)
  2. Enhanced migration & re-stimulation properties
  3. Survival / maintenance of those clones (respond to growth, survival signals)
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5
Q

What happens to the cd4+ cells stimulated by antigens?

A

Increase in numbers (Proliferation, clonal expansion)
Produce survival factors & cytokines (IL2, IFNg/IL4)
Change surface protein expression (adhesion molecules, chemokine receptors, activation markers)
Acquire effector functions: B cell help, CTL help, Macrophage help

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6
Q

What are the 2 possible pathways for generation of memory t cells?
(we’re not sure which is right)

A
  1. Divergent- 90% turn into effector cells, 10% into memory

2. Linear development- naive cell becomes effector cell and then when there’s no antigen some become memory cell

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7
Q

How are memory t cells maintained?

A

Most activated t cells are programmed to die- activation induced cell death (AICD)
Memory cell survival and maintenance is mediated by IL15 and IL7.

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8
Q

Which key cytokine drives the proliferation of effector t cells?

A

IL-2

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9
Q

Which cytokines maintain memory cell survival?

A

IL15 and IL7

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10
Q

How long have we found b cells can last?

A

90 years found

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11
Q

What was the first vaccination made from?

A

From cowpox virus. for smallpox.

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12
Q

Why don’t malaria, HIV and TB have vaccines? (when they’re so deadly)

A
Hard to get natural immunity to these.
People have latent diseases.
Complex life cycle.
Pathogen antigen variability.
transport, cost etc. measles is heat-sensitive
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13
Q

What’s the problem when people don’t trust vaccines?

A

When people are scared of vaccines, some don’t take the vaccine and it cannot be eradicated.
E.g. measles has come back in USA

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14
Q

Explain herd immunity

A

certain proportion must be immune to protect the rest of the population from that pathogen.
Depends on virulence of pathogen or susceptibility of population

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15
Q

What are the types of modern vaccines?

A
  1. related, less harmful infection e.g. cowpox
  2. killed or inactivated pathogen e.g. polio
  3. live attenuated pathogen e.g. MMR
  4. subunit (purified or recombinant components)
  5. conjugate (take an antigen and link it to bacteria that wouldn;t produce as much response
  6. Taxoid vaccine- some bacteria secrete toxins. use similar strategies to inactivate a vaccine, promotes body to make antibodies that can deal with toxins.
  7. virus-like particles
  8. genetic/dna vaccine
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16
Q

How can we improve vaccines?

A

Adjuvants
helper chemicals boost immune response to antigen
stimulate inflammation and antigen presentation to T clls.
Can increase immune response BUT can cause adverse immune pathology including organ damage, autoimmunity etc.

17
Q

What other conditions can we look to use vaccines in?

A

cancer? e.g. hpv and others caused by infectious agents

addictions? neutralise the drug and prevent high

reproduction? reversible contraceptive immune response against hCG