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Immunology > Antibodies and B-cells > Flashcards

Antibodies and B-cells Flashcards

1
Q

B-cell development in adults

A

bone marrow

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2
Q

b-cell development in fetus?

A

yolk sac and liver

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3
Q

6 phases of B-cell selection

A
  1. Making competent B-cells in bone marrow
  2. Negative selection
  3. Positive selection
  4. Searching for infection
  5. Finding infection
  6. Attacking infection
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4
Q

Markers on stem cell–> pro-B-cell

A

Stem cell= CD34
Lymphoid Progenitor= CD34, CD7, CD10,
B-Cell precursor= IL-7Ra, CD10

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5
Q

Induction of B-cell development

A

Stromal cells in bone marrow release IL-7

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6
Q

B-cell first makes?

A

heavy chain of antibody

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7
Q

Heavy chain production

A

Early pro-B cell= DJ recombination on BOTH chromosomes
Late Pro-B= V-DJ recombination one one chromosome. Success= inhibition of other segment.
50% cells undergo apoptosis

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8
Q

How many chances for IgH rearrangement?

A

2

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9
Q

Pro B cells vs Pre-B cell?

A

Heavy chain of antibody (mu antibody) is formed in Pre-B-cell. Associates with surrogate light chain

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10
Q

Pre-B cell needs to?

A

make light chain to become Immature B-cell

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11
Q

Light chain rearrangement

A

Kappa chain rearrangement (tried on both chromosomes) followed by lambda if both kappas fail
90% of cells undergo apoptosis here.

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12
Q

Allelic exclusion

A

Occurs in pro and pre-b-cells (heavy and light chain)
makes sure Ab only have one specificity. (two heavy chains don’t pair together). If one allele successfully does recombination, it prevents the rearrangement of the other alleles.

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13
Q

Difference between heavy and light chain rearrangement

A

heavy chain rearrangement has the diversity region, limiting number of recombination attempts. In light chain synthesis, each allele kappa and lambda get 5 tries before they die.

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14
Q

Pro-B-cell–> pre b-cell

pre b-cell ==> immature b-cell

A

addition of heavy chain (with temporary surrogate chain)

addition of light chain

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15
Q

Immature B-cells undergo

A

negative selection before they can leave the bone marrow.

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16
Q

Negative selection

A

Immature B-cells with self-reactive antibodies to MULTIVALENT self antigens cannot leave bone marrow. Light chain rearrangement starts up again= RECEPTOR EDITING (assuming it has more combinations). If it can’t figure it out, apoptosis.

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17
Q

Anergy

A

Self reactive B-cells to MONOVALENT antigens express high IgD and lower IgM so they’re useless. They leave the bone marrow, circulate, but quickly die.

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18
Q

Naive B-cells need?

A

activation by antigen. Go to lymph node via HEV.

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19
Q

How do B-cells get into the lymph nodes?

A

CCL21 attracts b-cell to HEV
CCL21 and CCL19 attract b-cell into lymph node
CCL13 into primary follicle

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20
Q

Immature B-cell to mature B-cell?

A

In the primary follicle (of 2 lymphoid tissue), follicular dendritic cells secrete BAFF= b-cell activating factor. BAFF binds b-cell and makes it mature. Still not active.

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21
Q

Path of B-cell through lymph node?

A

enters afferent blood vessel==> HEV in paracortex==> moves to outer part (primary follicle) and interacts with follicular d-cell. Mature B-cell exits via efferent blood vessel and circulates

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22
Q

B-1 Cells

A

Make in the fetal bone marrow. Pretty weird, not much is understood about them. Part of early response= considered part of innate immune system.

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23
Q

B1-B2 cells reaction with antigens?

A 
B1= poly reactive- not specific to one antigen. High chance of cross reactivity. 
B2= somatic hypermutation makes them very specific.
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24
Q

Memory cells?

A

B2. B2= “classical” b-cells= memory or plasma.

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25
Q

create many lymphomas and leukemias

A

B1. Do not need T- cell activation.

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26
Q

IgM vs IgG on B1/B2?

A

B1= IgM»IgG B2= IgG»IgM

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27
Q

Primary location of B1/B2?

A 
B1= peritoneal and pleural cavities
B2= Secondary lymph organs
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28
Q

B-cell tumors in bone marrow

A

Lymphoid progenitor= Acute lymphocytic leukemia
Pre-B-cell= pre-b-cell leukemia
plasma cell= multiple myeloma

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29
Q

Peripheral B-cell tumors

A

Germinal center b-cell= Hodgkin’s lymphoma–found in lymph organs

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30
Q

B-cell activation requires. Where does this happen?

A

Occurs in lymph node

  1. Finds antigen (presented by follicular dendritic cell)
  2. finds T-cell
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31
Q

B-cell: antigen interaction

A

Ag binding
Bcell CR2: C3d Ag =phosphorylation of CD19==downstream signaling.
B-cell CD19 and CD81 mediate interaction

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32
Q

Cytoplasmic signaling into b-cell?

A

Ig-alpha and Ig-beta have longer cytoplasmic domains that participate in downstream signaling once IgM has bound antigen.

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33
Q

purpose of CR2 on B-Cell

A

lowers threshold for antigen so that fewer IgM molecules need to bind. . binds C3D.

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34
Q

Steps of B-cell activation (from inactive mature B-cell)

A

Proliferation, somative hypermutation & affinity maturation, isotype switching, plasma/b-cell development

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35
Q

Proliferation of B-cells occurs?

A

In germinal centers of lymphoid follicles (activated b-cell proliferation)

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36
Q

germinal center mantle zone has

A

non-activated b-cells

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37
Q

After B-cell finds antigen from DC in primary follicle, it?

A

goes into T-cell area to find a t-cell match. Then they go into the medullary cords for proliferation. Then they move into the primary follicle for expansion= germinal center.

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38
Q

Follicular dendritic cells have two crucial jobs

A
  1. Release of BAFF to make mature B-cells

2. Activate B2 cells (antigen specificity)

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39
Q

Follicular Dendritic cell lineage

A

fibroblast

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40
Q

After proliferation, B-cells undergo…

A

somatic hypermutation

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41
Q

Somatic hypermutation & affinity maturation

A

Somatic hypermutation of hypervariable region of new centrocytes changes antigen specificity. If Ab can still bind dendritic cell, it gets survival factors. If it can’t it dies.

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42
Q

B-cell: t-cell interaction?

A

B-cell part :: T-cell part (another name because it wouldn’t be medicine if things only had one name)
CD40 (BCR):: CD40L (T-cell ligand)
MHC II (with Ag) :: TCR (CD3)
B7(CD 80):: CD28

43
Q

What happens after somatic hypermutation?

A

Isotype switching. dependent on cytokine signaling.
IFN-gamma= IgG2a, IgG3
TGFb/IL5= IgA, IgG2b
IL-4= IgE, IgG1

44
Q

IL-4 secreted by?

A

TH2 cell

45
Q

Centrocyte (b-cell)==> plasma cell requires

A

IL-10. Plasma cells then go to the bone marrow

46
Q

Centrocyte + ___ = memory b-cells

A

IL-4 (TH2 cells)

47
Q

TI-1 antigen

A

T-cell independent antigen. Polyclonal activation of B lymphocytes.
Ex: LPS (binds TLR4)
DNA= TLR9

48
Q

TI-2 antigen

A

repeated epitopes cause significant cross linking = B-cell activation. Antigen (polysaccharide) is not processed. No CD4 activation. Can activate B1 and B2 cells.

49
Q

Can we make vaccines to TI2 antigens?

A

Yes! Stick polysaccharide on a protein. B-cell specific for polysaccharide so that the B-cell processes it. Antigen (polysaccharide + protein) is broken down and polysaccharide is broken down and presented to T-cell= => activation of B-cell ==> formation of plasma cell that makes Ab for polysaccharide

50
Q

How does IgA reach destination?

A

IgA= mucosal, must cross epithelium.
Polymeric Ig receptor transcytosis into mucus with or without IgA. Since it’s polymeric it can take IgM but usually IgA»>IgM. IgM + secretory component (the receptor) secreted into mucus together.

51
Q

IgG transport

A

IgG= into extravascular space (across endothelial cells), into fetus (across placenta)
Brambell Receptor= FcRB

52
Q

IgA types

A 
IgA1= 26AA. 
IgA2= 13 AA= less flexible, but more stable to proteases
53
Q

Dimeric IgA

A

Secretory component covers hinge to protect from proteolytic degradation. J-chain connects two IgA’s.

54
Q

IgA1 vs IgA2 (location, structure)

A

IgA1= longer hinge region. More flexible, more susceptible to proteolytic degradation. More common in upper GI and Respiratory tract where there’s less bacteria.

IgA2= shorter hinge. More common in colon because can tolerate high levels of bacteria.

55
Q

Brambell receptor

A

= FcRB. Moves IgG into ECM. Active transport.

56
Q

First Ab fetus makes? Ab levels at 0 and 9 months?

A

IgM.
0 months= fetal IgM= maternal IgG&raquo_space; fetal IgG
9 months= fetal IgM>IgG> IgA. no more maternal IgG

57
Q

Purpose/Functions of Antibodies

A
  1. Neutralization
  2. Opsonization
  3. Complement Activation
58
Q

Neutralization

A

Ab binds antigen to prevent it binding to host cell.

Ex: IgA binds influenza.

59
Q

Bacterial toxins

A

AB receptor on antigen
A- active
B- binding.
B binding allows A to poison cell.

Neutralization inhibits B-binding to host cell.

60
Q

Fc Receptors

A

Link innate and adaptive immunity. Innate immune cells express Fc receptors in order for adaptic immune cells to bind.

61
Q

Fc(gamma)R- binds what? found on which cell(s)? plays a role in?

A

Bind IgG
Expressed on neutrophils, macrophages, B-cells, follicular cells, Dendritic cells and NK cells
Plays a role in: opsonization, NK ADCC

62
Q

Fc(epsilon)R- binds what? found where? plays a role in?

A

Binds IgE

Found on mast cells and basophils. Plays a role in allergic reactions. Binding==> cross linking==>degranulation.

63
Q

Fc(gamma)R1

A

high affinity receptor for IgG1 and IgG3

Receptor on macrophage binds CH2 domains of the IgG ab==>activation of phagocytosis.

64
Q

Main Fc on neutrophils and macrophages? NK cells?

A

Neutrophils and macrophages= Fc(gamma)RI (CD64)

NK cells= Fc(gamma)RIII (CD16)

65
Q

This IgG plays an anti-inflammatory role. Ratio of these two is what determines outcome of allergic response.

A

IgG4: IgE

66
Q

NK Antibody-dependent cell- mediated cytotoxicity

A

Fc(gamma) RIII= CD16 binds antibody bound to antigen.
Ex: Lymphoma has CD20 R, which binds Ab Anti-CD20. NK cell sees AntiCD20 and binds with its Fc(gamma)III R and elicits cell death.

67
Q

IgG with greatest Fc binding?

IgG in greatest concentration?

A

IgG3- longest hinge= greatest flexibility.1/2 life= 7 days

IgG1- most prevalent, 21 days

68
Q

Primary immune response produces?

A

low affinity IgM Ab

69
Q

Secondary immune response produces?

A

IgM+ naive B-cell that binds antigen is inhibited by Memory B-cell for that antigen. Therefore, secondary immune response results in production of high affinity IgA, IgG, and IgE. No time wasted on affinity maturation and stuff.

70
Q

B-lymphocytes cytokines in the bone marrow

A

IL 3,4,7

71
Q

Total surface receptors of a mature B-cell

A

IgM, IgD, class II MHC, CR1, CR2, Fc, CD19, CD20

72
Q

When macrophages secrete IL10…

A

TH2 response= B-cell proliferation, anti inflammatory response.

73
Q

What regulates light and heavy chain recombination?

A 
RSS= recognition signal sequence. 12 bp space must combine with 23 bp spacer. 
12= V
23= J
74
Q

What does RAG do

A

during recombination, RAG bring V+J together.

RAG recombinase cuts out the middle part and joins VJ

75
Q

Diversity is added by?

A

TdT= N-nucleotide addition. Random addition of bases.

76
Q

switching between IgM and IgD

A

= RNA splicing. VDJ regions remain the same so the antigen specificity is unaltered.

77
Q

Membrane vs secreted IgM from?

A

alternative splicing

78
Q

Alternative splicing does 2 things

A
  1. IgM vs IgD

2. transmembrane Ab vs secreted Ab

79
Q

Somatic hypermutation

A

AID (activation induced cytosine deaminase) adds uracil randomly. Uracil is a mistake (working with DNA) so it is replaced randomly with another base.

80
Q

Hypervariability regions

A

regions of IgM/IgD light and heavy chains with high variability. 2 weeks after immunization, CDR1 has highest variation.
CDR1, CDR2, CDR3= hypervariability regions. Determine Ag binding specificity.

81
Q

AID mediates 2 things

A

Activation induced cytosine deaminase.

  1. Somatic hypermutation
  2. Isotype switching
82
Q

Isotype switching AID

A

AID targets switch regions and results in new Ab production

83
Q

IgM structure/Function (4)

A

secreted as pentamer (usually). No hinge region, 4HC domains

  1. Most important mucosal Ab.
  2. First Ab made during primary immune response
  3. Activation of compliment cascade
  4. Agglutination
84
Q

How does IgM make up for it’s low affinity to antigens?

A

Pentamer= lots of binding spots= higher avidity

85
Q

IgG structure/ Function

A 
Four subclasses, 
Activate complement (IgG3>1>2) NOT IgG4!
Opsonization via Fc receptor binding
86
Q

IgG subclass structure comparisons

A

IgG3= longest hinge, highest flexibility, increased susceptibility to proteases= shortest 1/2 life

87
Q

Monovalent IgG? What induces this?

A

IL-4
Monovalent= binding only ONE antigen.
IgG4- can dissociate at hinge, and combine with another IgG4 with different antigen specificity, thereby reducing the ability of IgG4 to bind with two antigens. Decreased effectivity= dampened immune response= ANTI INFLAMMATORY

88
Q

Bivalent antibody

A

All of them. Except IgG4. And IgM is supervalent (pentamer= 10 binding spots)

89
Q

IgA– what cytokine promotes IgA

  1. Structure
  2. Functions
  3. Weak to? (ex of pathogens and why it’s weak)
A

IL-5

  1. dimer w/ J chain that increases stability
  2. Does not activate compliment effectively. Works to neutralize bacteria in intestinal and respiratory tract by cross-linking to prevent their entry.
  3. S. Pneumonia, Hemophilus influenza, m. meningtiidis make proteases that cleave IgA. (ie resistant to Iga)
90
Q

IgE

  1. Normal serum concentration
  2. Structure
  3. Function
A

IL-4

  1. Very low in normal people. Marker for allergies (US) and parasites (aka HELMINTH–in 3rd world countries)
  2. Extra CH (constant heavy domain) and no hinge region
  3. Binds FcEpsilon receptor on mast cells and basophils to induce cross linking and degranulation= release of inflammatory mediators.
91
Q

IgD

  1. Serum concentration
  2. Structure
  3. Main location
A
  1. Very low
  2. same as IgG, 2 heavy chains (3Hc, 1Hv) 1 light chain. Hinge present
  3. IgD secreting plasma cells in URT. Function isn’t really known because knockout mice don’t show symptoms. Assumed to help protect URT, though.
92
Q

Heaviest Ig

Most prevalent Ig

A

Heaviest: IgM- pentamer= 970kDa

Highest concentration: IgG1

93
Q

Best antibodies for neutralization?

A

IgG1,2,3,4 and IgA

94
Q

Best Ab for opsonization?

A

IgG1, IgG3

95
Q

Activators of NK cells? (ab)

A

IgG1, IgG3

96
Q

Activation of mast cells? (which Ab)

A

IgE

97
Q

Activation of complement system? (which Ab)

A

IgM, IgG1, IgG3

98
Q

Epithelial transport of Ab?

A

IgA»>IgM

99
Q

Placental transport of Ab?

A

IgG1> IgG3, IgG4»IgG2

100
Q

Diffusion into tissue (extravascular sites)? (Ab)

A

IgG’s>IgA>IgE&raquo_space;>IgM (depends on if it’s a pentamer)
Pentamer IgM cannot diffuse
FYI: Air can, from zone 17-23

101
Q

Ig Genes are rearranged a lot during a B-cells life cycle….What mechanisms are reversible?

A
  1. IgM IgD switching- Why? It’s via RNA splicing, not DNA

2. Secreted vs surface Ab on B-cell- again, RNA splicing, not DNA recombination

102
Q

What promotes IgG1/IgG3 class switching?

A

IFN-gamma

103
Q

How does B-cell down regulate T-cell activity

A

This is from core:
B7 (CD80/86):: CTLA-4

No idea what all that really means…

Immunology (12 decks)

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