Brainscape's Knowledge GenomeTM

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


See full index

Population Dynamics > Population dynamics in immunology > Flashcards

Population dynamics in immunology Flashcards

Lectures: -L6 - T- & B-cell diversity & selection -L7 - Host diversity

1
Q

How can T- & B-cell diversity occur on an intra-individual level? (2)

A
  1. IGR/TCR recombination
  2. Somatic hypermutation (B-cells only)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How can T- & B-cell diversity occur on an inter-individual level? (2)

A
  1. Antigen receptor gene polymorphisms
  2. HLA polymorphisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the definition of ‘repertoire’ (as in B-cell or T-cell repertoire)?

A

All productive IG/TR rearrangements

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

What are two key aspects for productive IG/TR rearrangements?

A
  1. Triplet coding
  2. Reading frame
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How many reading frames do the V-, J- & D-genes have?

A

V-genes: single reading frame
J-genes: single reading frame
D-genes: multiple reading frames

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

What part of IG/TR rearrangements is productive?

A

~1/3

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

What are reasons for non-productive gene rearrangements? (2)

A
  1. Use of non-functional gene regions
  2. Problematic junctions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is often the problem in non-functional gene regions that cause non-productive rearrangements? Where are they often located?

A

They often contain stop codons
Often located in V-genes

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

What is an alternative name for non-functional gene regions that cause non-productive rearrangements?

A

Pseudogenes

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

Which 3 mechanisms can cause problematic junctions result in non-productive rearrangements?

A
  1. Out of frame (number of nucleotides addes was not 3 or a multiple thereof)
  2. Junctions carrying stop codons (introduced during nucleotide addition)
  3. Absent CDR3 anchors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are CDR3 anchors? How can absent CDR3 anchors cause non-productive gene rearrangements?

A

Preserved sequences that produce amino acids on specific positions, which are needed for a correct receptor structure
When these amino acids are substituted, the receptor structure won’t be correct

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

After gene rearrangement, productive gene rearrangements can still become non-productive. How?

A

As a result of somatic hypermutation, the functional rearrangements could be changed in such a way that they do not produce a functional protein anymore

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

Productive rearrangements can be analyzed on DNA, RNA and protein level. What is the (approximate) ratio of functional vs. non-functional rearrangement on each of these three levels?

A

DNA-level: 1/3 productive, 2/3 non-productive
RNA-level: mostly productive
Protein level: almost exclusively productive

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

Productive rearrangements can be analyzed on DNA, RNA and protein level. How can the (approximate) ratio of productive vs. non-productive rearrangements on DNA-level be explained?

A

1/3 productive & 2/3 non-productive can be explained on the basis of triplet coding -> only introduction of (a multiple of) 3 nucleotides results in productive rearrangements -> chance of about 1/3

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

Productive rearrangements can be analyzed on DNA, RNA and protein level. How can the (approximate) ratio of productive vs. non-productive rearrangements on RNA-level be explained?

A

On RNA-level, we find mostly productive rearrangements
This is skewed towards productive rearrangements due to the preselection of transcription of productive gene rearrangements

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

Productive rearrangements can be analyzed on DNA, RNA and protein level. How can the (approximate) ratio of productive vs. non-productive rearrangements on a protein level be explained?

A

On protein level, we find almost exclusively productive rearrangements, because non-productive recombinations rarely make it into the protein stage

17
Q

Some compartments will have a higher amount of productive vs. non-productive rearrangements. Which compartment contains a relatively high percentage of productive rearrangements? Why?

A

Lymph nodes/spleen -> only cells with productive rearrangements get to this stage

18
Q

Some compartments will have a higher amount of productive vs. non-productive rearrangements. Which compartment contains a relatively low percentage of productive rearrangements? Why?

A

Bone marrow/thymus -> these contain B-/T-cells in early development

19
Q

On which levels can antigen receptor diversity be studied? (2)

A
  1. DNA-/RNA-level, using molecular techniques
  2. Protein level, using (mostly) flow cytometry
20
Q

Which resolutions of analysis of the antigen receptor diversity can be studies at DNA-/RNA-level? Which technique would be used?

A
  1. Low resolution using Sanger sequencing
  2. High resolution using NGS
21
Q

Why would we use low resolution Sanger sequencing when studing antigen receptor diversity? What information does this technique give us?

A

To get an impression of antigen repertoire and its diversity
This technique can be used to check for size differences between gene sequences -> size differences represent differences in the length of the junctional region, as the other regions are preserved

22
Q

Why would we use high resolution NGS when studing antigen receptor diversity? What information does this technique give us?

A

It can be used to study the whole region between the V- and J-sites of a large amount of cells -> gives a full picture of the diversity of combinations

23
Q

Which two techniques are available to study antigen receptor diversity on a protein level?

A
  1. Antibody-based techniques
  2. Labelled antigens/tetramers aimed at specific receptors
24
Q

What is the advantage of antibody-based techniques when studying antigen receptor diversity on a protein level? What causes this?

A

Recognize families of receptors
They do this because these antibodies are not specific enough to distinguish between individual receptors

25
Q

What is the disadvantage of antibody-based techniques when studying antigen receptor diversity on a protein level?

A

They are mostly available for TCR’s, not so much for IGR’s

26
Q

What is the advantage of using labelled antigens/tetramers when studying antigen receptor diversity on a protein level?

A

They have a high receptor specificity

27
Q

When would we use labelled antigens, and when would we use tetramers when studying antigen receptor diversity on a protein level?

A

Labelled antigens for immunoglobulin receptors/antibodies
Tetramers for TCR

28
Q

Which two dynamics can be seen in the B-/T-cells and their receptors?

A
  1. From naïve in the bone marrow to selected repertoire in the periphery due to maturation and differentiation
  2. Ontogeny -> during life the receptor repertoire gets skewed towards certain pathogens
29
Q

Which 2 dynamics occur to B-cells at a cellular level during life?

A
  1. Changes in output from the bone marrow
  2. B-cell memory formation
30
Q

How does the output of B-cells from the bone marrow change during life?

A

Higher at the start of life (first few years), lessens as the compartment gets filled

31
Q

Which two ‘factors’ of B-cell memory formation can be described as dynamic?

A
  1. Phenotypic differences -> most are CD27+, some are CD27-
  2. Place of formation
32
Q

Where can B-memory cells form? At which locations do/don’t they undergo class switch?

A
  1. Germinal centre -> undergo class switch
  2. Marginal zone -> do not undergo class switch
  3. Peripheral tissues -> do not undergo class switch
33
Q

Which 2 dynamics occur to B-cells at a molecular level during life?

A
  1. Ig-repertoire selection
  2. Ig-repertoire maturation
34
Q

What is Ig-repetoire selection? Towards which 2 characteristics is this selection?

A

Memory cells have a less diverse repetoire than naïve cells, causing a skewing/selection of the repertoire to occur

This skew is towards:
-Certain specificities/pathogens
-Towards shorter CDR3-regions

35
Q

What two processes occur during Ig-repertoire maturation?

A
  1. Selection against some Ig-genes as memory cells develop
  2. Selection of advantageous SMH mutations
36
Q

Which genes (V/D/J) are typically selected against during Ig-repetoire maturation & memory formation?

A

Certain V-genes

Population Dynamics (5 decks)

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