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Immunology > Exam II (generation of antibody diversity + B cell development) > Flashcards

Exam II (generation of antibody diversity + B cell development) Flashcards

1
Q

opsonin

A

any molecule that enhances phagocytosis by tagging it for binding to a cell surface
receptor

  • complement proteins that bind complement receptors
  • antibodies that bind Fc receptors on phagocytic cells
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2
Q

opsonization

A

“the process by which bacteria are altered by opsonins so as to become more readily and more efficiently engulfed by phagocytes”

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3
Q

what is the difference between an antibody being able to activate complement and acting as an opsonin?

A

IgG - complement activation and works with the complement receptor to induce phagocytosis

IgG - can also work as an opsonin itself by binding to Fc receptors on surfaces of certain phagocytes

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4
Q

most abundant isotype

A

IgG

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5
Q

combinatorial diversity

A

multiple germ line segments

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6
Q

generation of antibody diversity is due to:

A
  1. combinatorial diversity
  2. Junctional diversity
  3. Somatic hypermutation
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7
Q

human immunoglobin gene germline configuration

A
  • in all cells except for developed lymphocytes, immunoglobin DNA exists in this configuration
  • all loci are on 3 different chroosomes
  • composed of three types of gene segments V (variable), J (joining) and within the heavy chain locus D, (diversity) segment
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8
Q

two types of light chains

A

kappa and lambda

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9
Q

a heavy chain will unite with EITHER

A

kappa OR lambda

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10
Q

Recombination occurs in a precise series of steps

A
  1. Heavy chain begins rearrangement. The D to J segments are joined. Next, the joining of the V segment to the DJ segment. This locus is now ready to be transcribed (VDJ)
  2. After the heavy chain undergoes recombination, the light chain undergoes rearrangement. Since there are no D segments in the light chain, the only recombination is joining the V to J. This locus is now ready to be transcribed. Allelic exclusion also applies to the light chain as well.
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11
Q

antigen binding site heavy chain

A

VDJ

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12
Q

Antigen binding site light chain

A

VJ

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13
Q

allelic exclusion

A

only one B cell receptor will be expressed by any one B cell

applies to both heavy and light chain

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14
Q

Sequence of events during VDJ recombination

A
  1. Synapsis
  2. Cleavage:RAG1/2
  3. Hairpin Processing: artemis
  4. Joining
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15
Q

Synapsis

A

two selected coding segments and their adjacent RSSs are brought together by chromosomal looping

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16
Q

cleavage: RAG1/2

A

complexes generate ds breaks in DNA, forming hairpin loops

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17
Q

Hairpin processing: Artemis

A

Artemis opens hairpins at coding ends

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18
Q

Joining

A

non-homologous end joining

Ku70, Ku80, DNA ligase

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19
Q

RSS

A

recombination signal sequence

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20
Q

VDJ recombination is reversible/irreversible?

A

Irreversible

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21
Q

VDJ (heavy chain) and VJ (light chain) can be found in

A

the majority of the variable region - near amino terminus

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22
Q

types of combinatorial diversity

A
  • multiple gem line gene segments
  • multiple heavy and light chain pairings
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23
Q

Junctional diversity occurs at

A

CDR3 region -> allowing greater variability

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24
Q

junctional diversity increases diversity by

A

addition of nucleotides.
Can generate antibodies that have different amino acids

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25
Q

TdT

A

terminal deoxynucleotidyl transferase

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26
Q

TdT funciton

A

mediates junctional diversity - additional of nucleotides between the junctions of gene segments VDJ

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27
Q

the aa inserted by junctional diversity are inserted

A

between the V D J junctions (in between these)

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28
Q

N nucleotide addition

A

are added to both strands, at the junction (by TdT)

can potentially change the reading frame if the nucleotides aren’t a multiple of 3

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29
Q

P nucleotides

A

nucleotides complementary to the loose/uneven ends

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30
Q

V region assembly from gene fragments – somatic recombination of genomic DNA

A

irreversible

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31
Q

generation of junctional diversity – imprecision in joining rearranged DNA segments adds non-germline nucleotides (P and N) and deletes germ-line nucleotides

A

irreversible

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32
Q

assembly of transcriptional controlling elements –promoter and enhancer are brought closer together by V region assembly

A

irreversible

33
Q

Transcription activated with coexpression of surface IgM and IgD –two patterns of splicing and processing RNA are used

A

reversible and regulated

34
Q

synthesis changes from membrane Ig to secreted antibody –two patterns of splicing and processing RNA are used

A

reversible and regulated

35
Q

somatic hypermutation – point mutation of genomic DNA

A

irreversible

36
Q

isotype switch – somatic recombination of genomic DNA

A

irreversible

37
Q

events that happen in the formation of B cell receptor

A
  1. combinatorial diversity
  2. junctional diversity
38
Q

event after rearrangement and activation

A

somatic hypermutation

39
Q

Phase 1 - generation of diverse and clonally expressed B cell receptors in the bone marrow

A

repertoire assembly (BM)

40
Q

Phase 2 - alteration, elimination or inactivation of B cell receptors that binds to components of the human body

A

negative selection - BM

41
Q

phase 3 - promotion of a fraction of immature B cells to become mature B cells in the secondary lymphoid tissues

A

positive selection

( secondary lymphoid organs )

42
Q

Phase 4 - recirculation of mature B cells between lymph, blood, and secondary lymphoid organs

A

searching for infection

43
Q

phase 5 - activation and clonal expansion of B cells by pathogen derived antigens in secondary lymphoid tissues

A

finding infection

44
Q

phase 6 - differentiation to antibody secreted plasma cells and memory B cells in secondary lymphoid tissue

A

attacking infection

45
Q

sites of B cell development and response

A

bone marrow - B cell receptor is formed/assembled + NEGATIVE selection

if a B cell is not strongly reactive to self, it will move to secondary lymphoid organs (spleen, lymph node), where they can get activated

45
Q

sites of B cell development and response

A

bone marrow - B cell receptor is formed/assembled + NEGATIVE selection

if a B cell is not strongly reactive to self, it will move to secondary lymphoid organs (spleen, lymph node), where they can get activated

46
Q

stem cell in BM

A

u germine (H)
K/L germline (L)

47
Q

Pro B Cell in BM

A

uDJ (mu - heavy chain)
K/L germline, light chain

48
Q

Pre B Cell in BM

A

muVDJ
K/L germline, light chain

49
Q

pre b cell receptor

A

heavy chain can be tested for the ability to pair with a light chain - indicates productive rearrangement has occurred

50
Q

Immature B cell

A

muVDJ (H)
K/L - VJ

We now have a heavy chain (mu) + light chain fully rearranged

51
Q

Signal from a properly assembled Pre-B cell receptor induces

A

allelic exclusion at other heavy chain locus

52
Q

surrogate light chain

A

pairs with heavy chain, in order to test the heavy chain (IgB,A next to heavy chain)

53
Q

Surrogate light chain consists of

A

VpreB
Lambda 5

invariant molecules

54
Q

fully formed B cell receptor

A

has both heavy and light chains + associated with IgBeta and IgAlpha

55
Q

Immature B cell (in the secondary lymphoid organs)

BEFORE ACTIVATION

A

alternative splicing to give both delta and mu chains - IgD and IgM

56
Q

Antigen activated B lymphoblast (in the secondary lymphoid organs)

AFTER ACTIVATION

A

Alternative splicing to secrete Ig

Isotype switching

Somatic hypermutation

57
Q

An antigen activated B lymphoblast can become an

A

antibody secreting plasma cell (lose cell surface expression) OR memory cell (maintain cell surface expression)

58
Q

somatic hypermutation is induced by

A

AID

Activation Induced Cytidine Deaminase

59
Q

somatic hypermutation results in

A

point mutations, most often within variable regions of immunoglobins after rearrangement

60
Q

somatic hypermutation leads to

A

affinity maturation in the antigen-specific B cell pool

61
Q

Somatic hypermutation gives rise to affinity maturation of the B cell response to antigen

A
  • After activation, B cells undergo clonal expansion
  • Some clones will experience mutations in the antigen binding site that enhance antigen binding
  • Other clones will sustain mutations that reduce the affinity of the antigen binding site for antigen
62
Q

selection depends on

A

T cells! T cells need MHC to be able to recognize antigens.

63
Q

Increased affinity leads to

A

increased antigen uptake, processing and presentation.. leading to this cell getting more help from T cells

this cell, with increased affinity, will undergo clonal expansion

64
Q

transcription produces local single stranded DNA

A

in B cells, AID attacks cytidine in ssDNA to produce uridine

65
Q

AID also mediates

A

isotype switching

66
Q

isotype switching

A

changes the constant region of the heavy chain.

c(U), c(d), c(gamma).

last one to be switched to is Calpha2

67
Q

Isotype or class switching

A
  • happens after B cell activation in proliferating B cells
  • like somatic hypermutation, isotype switching is also dependent on AID
  • causes irreversible changes in DNA, removing intervening C regions
  • However, remaining C regions should still be used in subsequent switches
68
Q

AID responsible for

A

somatic hypermutation and isotype switching

69
Q

S(mu) + Sgamma1

A

AID has to act at these sites for isotype switching

70
Q

Lack of RAG leads to

A

SCID - no T cells or B cells can be produced

71
Q

Lack of TdT leads to

A

significantly reduced diversity in B cells repertoire

72
Q

Lack of AID leads to

A

no somatic hypermutation or isotype switching, produce only low affinity IgM, called hyper IgM immunodeficiency

73
Q

Events that rely on changes in DNA

A

Somatic Recombination

Junctional Diversity

Somatic Hypermutation

Isotype Switching

74
Q

Events that rely on changes in RNA

A

Dual expression of IgD and IgM

Expression of transmembrane vs secreted forms of IgM

75
Q

IgM and IgD (getting rid of either)

A

are changes in RNA due to differential splicing NOT changes in DNA. All C regions are maintained in the DNA at this point

No class switching has occurred yet.

76
Q

negative selection

A

in bone marrow - primary organ

77
Q

positive selection

A

secondary organs

Immunology (18 decks)

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