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Immunology > Lecture 8 - Immunity & B cells and AB's > Flashcards

Lecture 8 - Immunity & B cells and AB's Flashcards

1
Q

B cell activation requires what two signals?

A
  1. Antigen binding to the B cell receptor
  2. Th2 cell CD40L binding to the CD40 receptor on a B cell
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2
Q

What is the “third” signal that a B cell receives during activation?

A

Comes via cytokines, and determines whether the cell differentiates into a memory cell or a plasma cell

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3
Q

In order for antigens to signal B cell activation, what has to happen to the B cell receptors?

A

They must cross-link (with the antigens)

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4
Q

What is the purpose of having the Ig-alpha and Ig-beta coreceptors?

What is the next couple of steps?

A

They contain a longer cytoplasmic domain (ITAM) that gets phosphorylated (by Blk, Fyn, or Lyn)

Syk then binds to the ITAMS and is continues signal cascade

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5
Q

In addition to the IgM/Ig-alpha/Ig-beta of the B cell receptor, what other molecules are part of the B cell receptor complex?

A

Cr2

CD19

CD81

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6
Q

The CR2 molecule of the BCR complex binds to…

A

C3d o the bacterial cell

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7
Q

What happens after CR2 binds to C3d?

A

The CD19 molecule’s intracelular domain gets phosphorylated and a signal cascade occurs

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8
Q

Where do we find C3d?

A

On bacterial surface or bound to immune complexes (Ag/Ab complexes)

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9
Q

What type of B cells are BCR complexes expressed on?

A

All of them!

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10
Q

Which area of the lymph node has a high amount of proliferation?

A

The Dark zone of the germinal center

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11
Q

What makes up the mantle zone of the lymph node?

A

Non activated (naive) B cells

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12
Q

Antigens enter the lymph node via ____. B cells enter via _____.

A

Antigens = Afferent lymphatics

B cells = HEV’s

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13
Q

Antigen pathway once it gets to the lymph node

A

Afferent – subcapsular sinus – transport to follicle – binds to Follicular Dendritic Cells

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14
Q

The CR2 domain (yes, the same one that is part of the BCR complex) is also found on which cells?

A

Macrophages and Follicular Dendritic Cells

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15
Q

B cells are activated in the ______

By what?

A

paracortex

By a specific antigen that is presented by FDC’s in the T cell area

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16
Q

Antigen activated T cells __________

Antigen activated B cells move to _________

A

T cells proliferate and differentiate

B cells move to the boundary region and present antigen to effector TFH cells

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17
Q

What is formed when B cells present antigen to effector TFH cells?

A

Cognate interactions / Cognate pairs

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18
Q

The primary focus for expansion f antigen activated B cells is in the _________

The secondary focus for these cells is in the _________

A

Medullary cords

Primary follicle

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19
Q

Clonal expansion of the antigen-activated B cells occurs in ______, which creates _______

A

Primary follicle

Germinal center

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20
Q

Two surface molecules on FDC’s that bind and deal with virus/bacteria. Whats the main function of these?

A

CR1 and CR2

  • CR1 binds to C3b
  • CR2 binds to C3d

These bind to intact viruses and hold them at the surface.

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21
Q

Immature B cells (leaving) get what signal from FDR’s?

A

BFF

(induces maturation)

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22
Q

Somatic hypermutation occurs in the _____

It comes before _____, and that comes before ______

A

rapidly proliferating germinal center cells

SH -> Selection -> Affinity maturation

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23
Q

Affinity of the antibody will increase over time due to…

A

affinity maturation

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24
Q

If a B cell contains low affinity surface molecule in the germinal center, it doesn’t receive

A

survival signals from the FDC’s

…undergoes apoptosis

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25
Q

Isotype switching begins with what signal?

A

CD40L (from TH2 cell)

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26
Q

Isotype switching from IFN gamma?

A

IgG2a, IgG3

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27
Q

Isotype switching from TGFb and IL-5?

A

IgA

IgG2b

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28
Q

Isotype switching from IL-4?

A

IgE

IgG1

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29
Q

What cytokine makes B cells differentiate into:

  • plasma cells
  • memory cells
A
  • IL10 -> plasma cell
  • IL-4 -> memory B cell
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30
Q

Why didn’t patient 2 have trouble expressing both IgM and IgD, despite his problems?

A

M + D are formed at the level of mRNA splicing

*not* recombination at the DNA level

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31
Q

Why did the patient make antibodies against the blood group antigens but not against tetanus toxoid?

A

Blood group antigens are IgM-mediated

antibodies to Tetanus toxoid would be IgG, which this patient can not form.

32
Q

What did Patient 2 have that kept his Ig’s from class switching?

A

Hyper IgM syndrome

33
Q

Hyper IgM syndrome is a ____ mutation of _____ molecule

What do these patients lack?

A

X linked mutation of CD40L

No germinal centers!

34
Q

T independent antigen 1 (TI-1) function and example

A

Polyclonal activation of B cells via a different receptor than Immunoglobulin

ex: bacterial LPS

35
Q

What does LPS, a T-independent antigen, bind to to activate the B cell?

A

TLR-4

36
Q

TI-2’s… What’s their structure and function?

A

Repetitive epitopes in the capsule of bacteria, made of polysaccharides or proteins.

They activate B-1 or B-2 cells by binding to the B cell co-receptor

37
Q

TI-2 can’t activate B cells when?

A

In patients under 5 years old.

38
Q

Athymic people can only form antibodies by what mechanism?

A

T-independent antigens

T-dependent response will NOT work because no thymus for T cell maturation

39
Q

TI-1 and TI-2 do not result in…

A
  • Isotype switching
  • Formation of memory cells
40
Q

How do you make a vaccine that will create a response to a bacterial polysaccharide (a TI-2), if it normally doesn’t elicit a B cell response in kids under 5?

A

Use polysaccharide-toxoid conjugate

  1. B cell receptor binds to the polysaccharide
  2. Conjugate is internalized, degraded
  3. Toxoid peptides are presented to Tcell, which then activates the B cell

**effectively turns it into a T cell dependent repsonse**

41
Q

Examples of conjugate polysaccharide vaccines

A
  • H. influenzae
    • Use tetanus toxoid
  • Strep Pneumo
    • Uses diphtheria protein
  • Neisseria M.
    • Use diphtheria toxoid/protein
42
Q

Strep pneumo

cell type, clinical presentations, number of serotypes, and vaccines

A
  • Gram+ coccobacillus
  • URT infection, Otitis Media, PNA, Meningitis
  • >90 serotypes
  • Polysaccharide vax (23), Conjugate vaccine in kids
43
Q

Serotypes of Strep pneumo have…

A

limited cross reactivity

44
Q

What are the two Ig’s that cross barriers, and what do they cross?

A

IgA crosses epithelial cell into mucosal secretions

IgG crosses endothelial cells into extravascular space, OR across the placenta to fetus

45
Q

IgG active transport is mediated by what?

A

The Brambell receptor

*FcRB

46
Q

Steps in IgA active transport

A
  1. bids basolateral poly-Ig receptor
  2. Endocytosed
  3. Transported to apical surface
  4. Receptor is cleaved and IgA is bound to secretory component

*The secretory component is a remnant of the poly-Ig receptor that was left behind after cleavage

47
Q

What happens to the secretory component during IgA deficiency disease?

What else do we see happen?

A

It increases in the lumen

IgM is also increased because the Poly-Ig receptor can bind to it also

48
Q

Difference in structure of IgA1 and IgA2

A

IgA1 has a hinge region that is twice as long

*Both can be monomeric OR dimeric

49
Q

Function of the secretory component?

A

It protects IgA from cleavage by proteases in respiratory tract

50
Q

Difference in IgA1/2 distribution

A

IgA1 = URT

IgA2 = GI system

(A2 is better suited to deal with bacterial enzymes due to shorter hinge region)

51
Q

Active transport of IgG across placenta from mom-baby begins and ends when?

A

Begins months before birth

The passively transferred maternal IgG is done by 6-9 months postpartum

52
Q

What’s the deal with maternal IgA?

A

IgA from the milk remains in the GI, and doesn’t circulate in the system

53
Q

Effector functions of AB

A

Neutralization

Opsonization

Complement activation

54
Q

Neutralization by AB is useful for preventing…

What specific ones?

A

Bacterial toxin poisoning of the cell

Toxins from: Diphtheria, Tetanus, Cholera, Staphylococcus

55
Q

Bacterial toxins comonly have what two domains

A

A+B

B binds the cell

A is released into cell after endocytosis – poison

56
Q

Two types of Fc receptors

A

Gamma and epsilon

57
Q

Fc gamma receptors are on what cells?

What do they cause?

A
  • PMN
  • MQ
  • B cells
  • FDC
  • NK

Opsonization in PMN and MQ

ADCC in NK cells

58
Q

What cells have FcE receptors? Function?

A

Mast cells and Basophils (the degranulators)

*have a role in Allergy response

59
Q

The Fcgamma receptor on PMN and MQ

What does it bind?

What happens next?

A

Fcγ-RI

High affinity for IgG1+3

(binds to the hinge region)

The bound IgG3 molecule then binds antigen with its variable domain that is sticking out, and causes signaling of phagocytosis

60
Q

Opsonization: 4 steps

A
  1. Antibody binds to bacterium
  2. antibodies on bacteria bind to Fc receptors
  3. cell engulfs it into the phagosome
  4. fuse with lysososome and is degraded
61
Q

Other names for FcγRI, FcγRII, and FcγRIII

A

I = CD64

II = CD32

III = CD16

62
Q

Which Fcγ receptor has highest binding to IgG1

A

Fcγ-RI (CD64)

63
Q

What are the two inhibitory Fcγ receptors?

A

(Fcγ) R2B2 + R2B1

64
Q

What are the two most effective classes of IgG for binding to the Fcγ receptors

A

IgG3 + IgG1

65
Q

ADCC (NK cells) is initiated by the interaction of what molecule/receptor

What is the second step

A

CD20 (on tumor or virus infected cell) + Anti-CD20 (free)

—> The NK cell will bind the Anti-CD20 and cross-link its Fc receptors (FcγRIII)

66
Q

What are the 2 phases of mast cell degranulation?

A

Resting = IgE is bound to FcERI receptor

Activated = multivalent antigen crosslinks the IgE antibodies —–> Degranulate

***This is why first formation of IgE isn’t as big of a problem, its the second exposure that causes the crosslinking and degranulation in serious allergic reactions.

67
Q

IgG4 has more of a ______ function

A

anti-inflammatory

68
Q

IgG3 is a strong complement activator because…

but…….

A

It has a long hinge region (flexibility)

but it is more susceptible to cleavage

69
Q

Strongest immunoglobulin molecules in activation of complement

A

IgM, IgG1, IgG3

70
Q

The ratio of ______ is important for an alergic response

A

IgG4 : IgE

71
Q

Formation of immature B cells is an ______ and _______ process

A

Ag-independent, Constant

72
Q

Mature, naive B cell can circulate for

A

3-8 weeks

*will die if they done contact an antigen with their Ag-specific receptors

73
Q

Activation takes place in the __________

Isotype switching takes place in _______

A

Paracortex

Germinal Center

74
Q

Primary and secondary immune response… initial AB response takes about _______

The secondary response (re-exposure) is ____ and _____

A

A week

Rapid and Stronger

*higher affinity AB made

75
Q

Better quality antibodies of the secondary exposure are a result of what process?

What does this mean in a cellular context?

A

Affinity maturation

B cells with low affinity Ig receptors will be given an inhibitory signal (FcγR2B1) that prevents production of low-affinity IgM antibodies

–> only produce high affinity IgG, IgA, IgE

Immunology (10 decks)

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