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Molecular Immunology > Antigen recognition (8) > Flashcards

Antigen recognition (8) Flashcards

1
Q

What complex recognises and aligns the RSSs adjacent to the gene segments to be joined?

A

RAG1 RAG2 complex.

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2
Q

What three steps occur once RAG1 and RAG2 have recoginsed and aligned RSS sequences?

A
  1. Endonuclease activity introduces 2 ssDNA breaks close to RSSs.
  2. A DNA hairpin is created at the segments to be joined and a flush ds break at the end of the heptamers.
  3. Blunt ends ligated to form a signal joint. Nicked sequence is repaired to form the coding joint.
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3
Q

How can sequence variability be achieved in the coding joint?

A

It can be nicked at various points and TdT can add or removed nucleotides.

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4
Q

Where does antigen independent B cell differentiation take place?

A

Bone marrow.

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5
Q

How many nucleotides can TdT add?

A

Up to 12. these form the N region.

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6
Q

When does TdT add nucleotides?

A

During heavy chain rearrangement. This happens in the antigen independent stage in the bone marrow.

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7
Q

What are the three stages of antigen independent B cell differentiation?

A
  1. Heavy chain gene rearrangement
  2. Light chain gene rearrangement
  3. Selection against self.
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8
Q

When is IgM expressed in B cell differentiation?

A

After light chain rearrangement in the bone marrow.

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9
Q

What happens in the secondary lymphoid tissue?

A

Somatic hypermutation- antigen dependant B cell differentiation.

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10
Q

What is expressed in antigen dependant B cell differentiation?

A

Virgin/ naive B cells express IgM or IgM and IgD.

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11
Q

Where does somatic hypermutation occur, apart from in mature B cells?

A

Throughout rearranged V regions. In mature B cells it seems to cluster around CDRs.

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12
Q

What is affinity maturation and where does it take place?

A

The selection of high affinity receptors. It takes place in the 2ndry lymhoid tissue.

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13
Q

What is thought to introduce mutations in somatic hypermutation?

A

AID- Activation Induced cytidine deaminase.

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14
Q

What happens in class switching?

A

Same recombined V regions associate with different constant region genes.

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15
Q

What is the purpose of class switching?

A

To allow for different loclisation or the induction of different effector functions.

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16
Q

What is specifically retained in class switching?

A

The antigen.

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17
Q

Where does recombination occur in class switching?

A

Switch regions.

18
Q

Is class switching reversible or irreversible?

A

Irreversible.

19
Q

Why is class switching different to VDJ joining?

A

Initiated by AID acting at switch regions.

20
Q

AID allows for class switching and acts at switch regions. What do these regions contain?

A

G rich tandem repeats.

21
Q

What does AID do?

A

Mutates C to U.

22
Q

Where is AID expressed?

A

Activated B lymphocytes/

23
Q

What is AID active on?

A

ssDNA.

24
Q

What does AID actively trigger and why is this good?

A

AID actively triggers DNA repair pathways. These are error prone leading to mutations which introduce additional variation.

25
Q

What two error prone mechanisms can AID induce?

A

Mismatch repair

Base excision repair.

26
Q

What does AID ultimately cause?

A

Somatic hypermutation.

27
Q

What do single strand nicks leading to double strand nicks cause?

A

Class switching.

28
Q

Is co-expression of IgM and IgD reversible?

A

Yes.

29
Q

How can B cells produce different classes of M and D immunoglobulin before class switching has occurred?

A

Differential transcriptional processing and splicing.

30
Q

What can differential processing of a primary immunoglobulin transcript control?

A

Whether the B cells produces membrane bound or secreted IgM.

31
Q

Does secreted or membrane bound IgM predominated as more B cells become active?

A

Secreted.

32
Q

What are the three key features of the A chain locus for TCR genes?

A
  1. LVa 70-80 copies.
  2. Ja - 61 copies
  3. Ca region
33
Q

What are the 7 key features of a B chain locus for TCR genes?

A
  1. LVb 52 copies
  2. DB1
    3: JB1 6 copies
  3. CB1
  4. DB2.
  5. JB2 x 7
  6. CB2
34
Q

Is the same recombination machinery used for TCR V region genes as it is for developing B lymphocytes?

A

Yes.

35
Q

Do V regions of B or T cell receptors not undergo somatic mutation?

A

T.

36
Q

What four features increase the diversity of TCR genes?

A
  1. Multiple copies of each V gene segement.
  2. alpha and beta chain combination.
  3. Junctional diversity
37
Q

Where is junctional diversity concentrated in in TCRS?

A

CDR3 of TCR alpha and TCR beta.

38
Q

1-5% of T cells are gamma/delta. How are these generated?

A

Gene rearrangement.

39
Q

What do gamma/delta TCRS have less of?

A

V region segments.

40
Q

What could compensate for gamma/delta TCRS fewer V region segements?

A

Junctional variability focused at CDR3.

41
Q

gamma/delta TCR are known to be more ‘antibody like’. What do they appear not to require?

A

Processing or presentation by MHC.

Molecular Immunology (9 decks)

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