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HDM - Final > Antibody Mediated Humoral Immunity - Bowden (Completed) > Flashcards

Antibody Mediated Humoral Immunity - Bowden (Completed) Flashcards

1
Q

What are the co-receptors of a B cell? 6

A

CD19

CD81

CR2 (CD21)

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2
Q

What are the two major subsets of B cells? 6

A

Follicular B cells

Marginal B cells

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3
Q

What is a marginal B cell? 6

A

Resides in the spleen

Identifies blood-borne polysaccharide Ags

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4
Q

What is a follicular B cell? 6

A

Recirculating B cells

Make up the majority of B cells

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5
Q

What happens each time a naive B cell enters a lymph node? 7

A

They receive a survival signal (FDC), if they don’t receive this signal they degenerate

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6
Q

What is the first B cell signal? 9

A

Ag binding to membrane-bound Igs

must occur with 2 or more BCRs to conduct the signal

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7
Q

How B cell intracellular signaling differ from T cell intracellular signaling? 9

A

The ONLY difference is the initial Src kinase that interacts with Igα and Igβ

Lyn
Fyn
Blk

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8
Q

Besides cross-linking with two membrane Ig’s how else can the first B cell signal be generated? 10

A

Cross-linking can occur between a mIg and CR2 (complement receptor)

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9
Q

What changes does a B cell undergo after binding Ag w/ two BCRs? 11

A

Expression of survival proteins

Increased B7 expression

Increase cytokine receptor expression

Increased CCR7 expression (integrin)

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10
Q

Newly activated B cells secrete low levels of what? 12

A

IgM

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11
Q

In T-independent B cell activation what is lacking? 13

A

No class-switching

No memory formed

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12
Q

What is the second signal for B cell activation? 14

A

CD40L - from T cell
Bound to
CD40 - from B cell
+ cytokines

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13
Q

What happens first, class switching or affinity maturation in B cells? 16

A

They both happen at the same time

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14
Q

After activation from T helper cell where do B cells head? 17

A

They change their chemokine receptors and head to the follicular area where germinal centers are established

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15
Q

In reference to B cells, what are the two functions of T helper cytokine secretion? 18

A

To induce heavy chain class switching

Augment B cell differentiation and proliferation

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16
Q

How does switch recombination happen in B cells? What causes this? 19

A

Caused by CD40:CD40L and cytokines

DNA of heavy chain is opened up and a different C region is expressed which will be a C region downstream because IgM/IgD are the first constant regions

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17
Q

What is affinity maturation? 20

A

Introducing point mutations in variable regions to raise their affinity to specific Ags

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18
Q

What enzyme facilitates affinity maturation (somatic hypermutation)? 20

A

AID - activation-induced deaminase

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19
Q

What does activation-induced deaminase do in Somatic hypermutation? 20

A

AID converts cytosine to uracil allowing for Ape I to create ds breaks in DNA

20
Q

After a B cell is activated and undergoes somatic hypermutation how is it able to survive within the lymph node? 23

A

If they’re able to bind a follicular DC presenting they will receive survival signals

21
Q

Speaking to B cells, which recognizes protein vs polysaccharide? Which produces memory cells? 25

A

T-dependent B cells –> memory, recognizes proteins

T-independent B cells –> lack of memory, recognizes polysaccharides

22
Q

What changes does a Plasma cell make to its cluster differentiation expression? 26

A

Decrease: CD19, 20, and HLA Class II
-they aren’t APCs anymore

Increase: CD27, CD38, and CD138

23
Q

What is the effector molecule of the humoral immunity? 26

A

Abs

24
Q

How are memory B cells able to survive for such a long time period? 28

A

By expressing more Bcl-2 (anti-apoptotic protein)

25
Q

What are the surface markers for Memory B cells? 28

A

CD27

CD45R

26
Q

What happens if Ags are fully bound to secretory IgG (IgG>Ag)? 30

A

If the Fc regions of IgG binds a BCR it shuts down and inhibits the B cell

Fc region bound by an Fc receptor on the B cell with a single ITIM

27
Q

What is the principle defense against extracellular pathogens? 32

A

Humoral immunity

28
Q

Which cells have Fc receptors on their cell surface? 34

A

NKs

Macrophages

B cells

29
Q

What is the primary Ab present in the blood? 34

A

IgG

30
Q

What Ab isotype is predominant in primary antibody response vs secondary? What about affinity? 35

A

Primary antibody response - first infection: Usually IgM>IgG with a lower average affinity

Secondary antibody response - second infection: Usually >IgG (IgA or IgE) with a higher average affinity

31
Q

What are the effector functions of Abs? 36

A

Neutralizes microbes and toxins

Opsonization & phagocytosis

Ab-dependent cellular cytotoxicity (NKs)

Inflammation

Lysis of microbes

32
Q

What two distinct functions does the Fc region serve? 37

A

It delivers Ab to inaccessible anatomical sites

Serve as a bridge between Ag and Effector cells for that Ags destruction

33
Q

What do C3b and IgG have in common? 38

A

Both act as opsonizer

34
Q

What FcRs have high affinity for Ig? What cells would these receptors be found on? 39

A

FcγRI (CD64) –> Macrophages, neutrophils, eosinophils

FcεRI –> mast cells, basophils, eosinophils

35
Q

What is Ab neutralization? 40

A

The idea that Abs can inhibit toxins and microbes simply by binding to them and stopping them from:

Binding receptors

Moving through membranes

36
Q

How does complement fulfill the role of waste management? 42

A

Erythrocytes bind immune complexes containing C3b and C4b with its CR1 receptor

Erythrocyte heads to spleen and liver

Phagocytes within liver and spleen remove complexes and RBC re-enters circulation

37
Q

What transports IgG from maternal circulation, across the placenta, into fetal circulation? 50

A

IgG Fc receptor bound by FcRn of the endothelial cell

38
Q

What’s the difference if the first signal for B cell activation comes from two membrane Igs or a membrane Ig and CR2? 10

A

If C3d (from C3b) binds CR2 and causes complement cross-linking the attached Ag will be 1000x more immunogenic (aka better activation of the immune system)

38
Q

What is one major way Abs resemble complement? 38

A

Abs bound to Ag can be bound by FcRs to act as opsonizers

39
Q

What FcRs have low affinity for Ig? 39

A

FcγRIIA (CD32)
FcγRIIB (CD32)
FcγRIIIA (CD16) - NK cells (Ab-dep. cellular cytotoxicity - ADCC)

40
Q

What does ADCC stand for? What state/condition is the body in when ADCC is active? 43

A

Antibody-dependent cellular cytotoxicity

Active when the body is in an anti-viral state

41
Q

What is the most effective fixer of complement (C’)? Why? 44

A

IgM becuase it contains five Fc regions that can be bound by CR receptors

42
Q

What is the therapeutic role of IVIg? How does it serve this role? 45

A

In treating autoimmune/inflammatory disease

Engages the inhibitory FcγRIIB (B cell) and the FcR of DCs suppressing the immune response

43
Q

What two Abs are lacking at birth and have a lag time of 6-12 months leaving the infant immunocompetent? 51

A

IgG and IgA (newly synthesized)

44
Q

What are three mechanisms of humoral immune evasion? 52

A

Ag variation - Ag not recognized

Inhibition of C’

Blocking via Hyaluronic acid capsule

HDM - Final (15 decks)

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