Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology > Memory and vaccines > Flashcards

Memory and vaccines Flashcards

1
Q

What are the key features of a secondary immune response?

A

1) Faster
2) Stronger
3) More effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the basis for vaccines?

A

Immunological memory; memory can be lifelong, meaning patient may not show any symptoms upon repeated exposure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the basis for vaccines?

A

Immunological memory; memory can be lifelong, meaning patient may not show any symptoms upon repeated exposure.

Vaccine immunise patients with benign form of pathogen to induce immunological memory against disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What was Edward Jenner famous for?

A

1780: vaccination against small pox (using cowpox)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What was Louis Pasteur famous for?

A

1880: Developed vaccines for chicken cholera, rabies and anthrax.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are mechanisms of immunological memory 1?

A

1) Long lived Plasma cells which produced continual low level circulation of specific antibodies.
2) Generation of memory lymphocytes during adaptive response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the characteristics of memory cells?

A

1) They are long lived

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the characteristics of memory cells which make them more efficient than naive Lymphocytes?

A

1) They are long lived; they survive even in complete presence of antigen
2) They are more sensitive to low doses of antigen than naive B/T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is essential for the survival of B cells?

A

prdm1 is the gene that encodes a transcription factor Lymph1 needed for survival.
No gene, means there is no memory cell marker called CD38; memory cell proliferation is low. When antigen (NP) added to knockout the response of memory cells is lower.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe an experiment to show memory cell sensitivity.

A

-purify naive and memory T cells
-immuno-labelling using Ab against T cell marker and conjagated Ab with gold particles
-stained cells with gold Ab
-visualised by electron microscopy
The memory cells have more clustered TCR, therefore more effective T cell activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the three characteristics of memory cells which make them more efficient than naive Lymphocytes?

A

1) They are long lived; they survive even in complete presence of antigen
2) They are more sensitive to low doses of antigen than naive B/T cells
3) Their response is faster and stronger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe an experiment to show memory cell sensitivity.

A

-purify naive and memory T cells
-immuno-labelling using Ab against T cell marker and conjagated Ab with gold particles
-stained cells with gold Ab
-visualised by electron microscopy
The memory cells have more clustered TCR, therefore more effective T cell activation
-increased activation shown by CD25 or secretion of T cell cytokine IFN-gamma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why are memory cells faster and stronger?

A

1) There is higher frequency of antigen-specific memory cells as a result of previous clonal proliferation; There is more!
2) They have already undergone isotype switching so memory cells are primed to make correct antibodies with the best affinity for antigen (hypermutation) and so more effective
3) It is only memory cells that take part

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why are memory cells faster and stronger?

A

1) There is higher frequency of antigen-specific memory cells as a result of previous clonal proliferation; There is more!
2) They have already undergone isotype switching so memory cells are primed to make correct antibodies with the best affinity for antigen (hypermutation) and so more effective for T cell binding.
3) It is only memory cells that take part to save time activating a naive B cell, when tried and tested B cell awaits.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the mechanism involved in secondary immune response.

A

Only emery cells participate.

-naive B cells bind to pathogen-Ab complex. Negative signal to naive B cell so it is not activaed, there is no production of its low affinity initial IgM Ab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the mechanism involved in secondary immune response.

A

Only emery cells participate.

  • naive B cells bind to pathogen-Ab complex. Negative signal to naive B cell so it is not activaed, there is no production of its low affinity initial IgM Ab
  • memory B cell binds to pathogen-Ab complex. Memory cell activated into plasma cell which makes correct (rearranged) Ab immediately.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the mechanism involved in secondary immune response.

A

Only emery cells participate.

  • naive B cells bind to pathogen-Ab complex. Negative signal from Fc-gammaRIIb (FcyRIIB) to naive B cell so it is not activaed, there is no production of its low affinity initial IgM Ab
  • memory B cell binds to pathogen-Ab complex. Memory cell activated into plasma cell which makes correct (rearranged) Ab immediately other than IgM.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is FcyR2B?

A

Inhibitory receptor which binds to IgG on naive B cells that prevents their involvement in the secondary response.

The receptor has ITIM as a signalling motif

FcyRIIB is downregulated on memory cells so these are not inhibited.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why are memory cells faster and stronger?

A

1) There is higher frequency of antigen-specific memory cells as a result of previous clonal proliferation; There is more!
2) They have already undergone isotype switching so memory cells are primed to make correct antibodies with the best affinity for antigen (hypermutation) and so more effective for T cell binding.
3) It is only memory cells that take part to save time activating a naive B cell, when tried and tested B cell awaits.
4) They are hypersensitive to antigen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the mechanism involved in secondary immune response.

A

Only memory cells participate.

  • naive B cells bind to pathogen-Ab complex. Negative signal from Fc-gammaRIIb (FcyRIIB) to naive B cell so it is not activaed, there is no production of its low affinity initial IgM Ab
  • memory B cell binds to pathogen-Ab complex. Memory cell activated into plasma cell which makes correct (rearranged) Ab immediately other than IgM.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is FcyR2B? How does it work?

A

Inhibitory receptor which binds to IgG on naive B cells that prevents their involvement in the secondary response.

The receptor has ITIM as a signalling motif; ITIM phosphorylated, so it recruit/docks phosphatases when which act to dephosphorylate signalling molecules and inhibit B cell activation.

FcyRIIB is downregulated on memory cells so these are not inhibited.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What experiment involving PKD can be used to show inhibitory FcyRIIb effect?

A

protein kinase PKD enzyme when activated in absence of FcyRIIB it autophosphorylates itself; activity measured in kinase assay.

PKD is blocked by engagement of the FcyRIIb receptor, despite initial autophosphorylation; activation signals are switched off over time.

Shows that negative ITIM dominates activation via BCR in naive B cell.

23
Q

Why are memory cells faster and stronger?

A

1) There is higher frequency of antigen-specific memory cells as a result of previous clonal proliferation; There is more!
2) They have already undergone isotype switching so memory cells are primed to make correct antibodies with the best affinity for antigen (hypermutation) and so more effective for T cell binding.
3) It is only memory cells that take part to save time activating a naive B cell, when tried and tested B cell awaits.
4) T memory cells are hypersensitive to antigen.

24
Q

What experiment involving PKD can be used to show inhibitory FcyRIIb effect in naive B cells?

A

protein kinase PKD enzyme when activated in absence of FcyRIIB it autophosphorylates itself; activity measured in kinase assay.

PKD is blocked by engagement of the FcyRIIb receptor, despite initial autophosphorylation; activation signals are switched off over time.

Shows that negative ITIM dominates activation via BCR in naive B cell.

25
Q

What features of memory T cells make them more sensitive?

A

1) enrichment of Oligomeric T cell receptor complexes

26
Q

What features of memory T cells make them more sensitive?

A

1) enrichment of Oligomeric T cell receptor complexes

2) They splice out CD45 mRNA so they express a different isoform

27
Q

What is the role of CD45 in T cells?

A

It is a phosphatase which dephosphorylates certain inhibitory sites on kinases so they become active.

Therefore, it is important for positive regulation of TCR signalling

28
Q

What are the 2 isoforms of CD45?

A
  • CD45RO: on effector and memory T cells. This CD45RO causes increased TCR signalling.
  • CD45RA: on naive T cells
29
Q

What features of memory T cells make them more sensitive?

A

1) enrichment of Oligomeric T cell receptor complexes
1) They splice out CD45 mRNA so they express a different isoform; they express CD45RO isoform which has lower activation threshold, stronger TCR signalling, and more rapid up-regulation of CD40L

30
Q

What are the 2 isoforms of CD45?

A
  • CD45RO: on effector and memory T cells. This CD45RO causes increased TCR signalling, and activating kinases.
  • CD45RA: on naive T cells
31
Q

Why are memory cells faster and stronger?

A

1) There is higher frequency of antigen-specific memory cells as a result of previous clonal proliferation; There is more!
2) They have already undergone isotype switching so memory cells are primed to make correct antibodies with the best affinity for antigen (hypermutation) and so more effective for T cell binding.
3) It is only memory cells that take part to save time activating a naive B cell, when tried and tested B cell awaits.
4) T memory cells are hypersensitive to antigen.
5) Memory T cells migrate to peripheral tissue so they are ready for activation at the site in tissue.

32
Q

What features of memory T cells make them more sensitive?

A

They splice out CD45 mRNA so they express a different isoform; they express CD45RO isoform which has lower activation threshold, stronger TCR signalling, and more rapid up-regulation of CD40L

33
Q

What makes memory T cells persit in perpherial tissues?

A 
Markers 
For adhesion: 
-CD44
For homing to lymph node: 
-CD62L
-CDR7
34
Q

What are the two subsets of memory T cells?

A

1) Central memory T cell: where CD62L and CCR7 in secondary lymphoid tissues only (still better at upregulating co-stimulatory CD40L)
2) Effector memory T cell: there is no CCR7 which means cell can exit lymphoid tissues into periphery liked mucosal. Here, re-exposure to antigen causes differentiation into effector T cells

35
Q

Describe an experiment that shows it is CCR7 that controls memory cell trafficking

A
  • memory T cell with low levels of CCR7 treated with drug rapamycin with increases CCR7 expression.
  • divide high CCR7 and low CCR7 populations and inject into a mouse
  • there is 50/50 distribution in blood, and more low CCR7 in secondary lymphoid tissues
36
Q

Describe history of vaccines

A

1885-1950: most of vaccines developed through trying to kill/inactivate pathogen but retain immunogenicity and inject this.

las 40 year: there have been new approaches involving genome sequencing to deermine proteins and biochemical analysis for immunogenicity tests

37
Q

Live-attenuated virus vaccines like Yellow fever, or polio vaccines

A

A live pathogen that can replicate in body but it no longer has pathogenicity.

Loss of pathogenicity due to mutation after serial growth in non-human cells; adapting to different host, and so it can no longer grow well in human cells

38
Q

What does attenuated refer to ?

A

pathogen can no longer grow well in human cells.

39
Q

list some advantage and disadvantages of live-attenuated virus vaccines

A

Advantages:

  • strong cellular/Ab response
  • lifelong immunity

Disadvantages:

  • needed to large doses, even multiple doses
  • pathogen can revert back to virulent form
  • cannot be given to weak immune system
  • temperature sensitive; in hot, poor countries hard to maintain.
40
Q

Inactivated virus vaccine like influenza

A

This is made from non-replicating viruses that inactivates nucleic acid but retains

41
Q

Inactivated virus vaccine like influenza

A

This is made from non-replicating viruses that inactivates nucleic acid so they cannot replicate (virus is dead) but retains antigenicity

42
Q

list some advantage and disadvantages of inactivated virus vaccines

A

Advantages:

  • safe
  • not temperature sensitive

Disadvantages:
-less strong immune response

43
Q

list some advantage and disadvantages of inactivated virus vaccines

A

Advantages:

  • safe
  • not temperature sensitive

Disadvantages:

  • less strong immune response
  • multiple doses required
44
Q

What are Subunit vaccines like Hepatitis?

A

These are made from antigenic components of a pathogen purified directly from pathogen or generated in lab.

Here, recombinant DNA technology has made the antigenic proteins more efficient.

45
Q

list some advantage and disadvantages of subunit vaccines

A

Advantage:

  • contain only the specific antigens needed
  • less adverse reaction/safer

Disadvantage:
-the appropriate antigen has to have been already isolated to be immunogenic.

46
Q

What is toxoid vaccine like tetanus?

A

These are made with chemically inactivated bacterial toxins that have retained their antigenicity

47
Q

What is toxoid vaccine like tetanus?

A

These are made with chemically inactivated bacterial toxins that have retained their antigenicity.

The toxins create the disease phenotype.

48
Q

What is conjugate vaccine like Hib (Haemophilus influenza type B)?

A

These are made by linking bacterial polysaccharide capsular antigens to a carrier.

49
Q

What is conjugate vaccine like Hib (Haemophilus influenza type B)?

A

These are made by linking bacterial polysaccharide capsular antigens to a carrier. These are effective against polysaccharide antigens.

50
Q

What are all the different types of vaccines?

A

1) Live-attenuated virus vaccines
2) Inactivated virus vaccines
3) Subunit vaccines
4) Toxoid
5) Conjugate

51
Q

Describe how a Hib toxoid vaccine works?

A

1) the vaccine is a combination of a polysacc. and the tetanus toxoid
2) B cell recognise polysacc part and internalise via endocytosis.
3) peptides made and toxin is separated, loaded on MHC2 and presented to helper T cell
4) IL4 from T cell means B cell differentiates, and expands.
5) Anti-polysaccharide Ab made

52
Q

Why are some vaccines not yet established for infectious disease like Tuberculosis?

A

1) pathogen Antigens mutate
2) pathogens have mechanisms to evade the immune system
(3) pathogen initiates a non-productive immune response.)

53
Q

How are we currently approaching the HIV vaccine? Why has it failed?

A

Failures include:

  • classical viral envelop antigens
  • dead HIV1 does not retain antigeniciy
  • live vaccines is too dangerous
  • vaccine does not defeat latent reservoirs of infection
  • The HIV is very mutable and rapidly changes under selection.
54
Q

What is the basis for vaccines?

A

Immunological memory; memory can be lifelong, meaning patient may not show any symptoms upon repeated exposure.

Vaccine immunise patients with benign form of pathogen to induce immunological memory against disease; it activates both T and B cells.

Immunology (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions