B Cells & Antibodies Flashcards

1
Q

The diversity of both chains of the BCR/antibody comes from…

A

rearranging gene segments on chromosome 14 (one from mom, one from dad)

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2
Q

Four different gene segments for BCRs

A

V, D, J, and C

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3
Q

T or F. Both chromosome 14 works to make a BCR

A

F! only the chromosome that gets a working combination gets the job! other chromosome shuts down

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4
Q

T or F. The Hc is produced first

A

T!

- process is repeated for Lc and Hc and Lc have to fit together as final test

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5
Q

Two interacting components of how a BCR signals

A
  1. pathogen is recognized by epitope (50-79 AAs long) binding to the Hc and Lc ‘antennae’
  2. proteins IgA and IgB transmit a signal to let the B cell know to turn on its Ab-making
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6
Q

The concept of cross-linking (how the BCR signals)

A
  1. polymeric antigen: repeats of an epitope can bind multiple BCRs and bring them together, also many copies of the same antigen can do this
  2. complement receptors on the B cell recognize a fragment of iC3b, enhancing the clustering that occurs with BCRs - amplifies B cell signalling by 100-fold; acts as a co-receptor
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7
Q

Second signals for B cell activation

A

with or without Th help!

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8
Q

What is the first signal in B cell activation?

A

cross-linking or clustering

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9
Q

The second or co-stimulatory signal for B cell activation is crucial as it determines the _______ of the B cell response.

A

quality

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10
Q

T cell-dependent activation second signal

A

CD40 on the B cell binds to CD40L on Th cell AKA CD154

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11
Q

T cell-independent activation second signal

A

involves interaction with a ‘danger signal’, most likely by recognition of PAMPs by Toll-like receptors or other PRRs

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12
Q

Advantages of T-independent B cell response

A
  1. fast; don’t need for Th cells to be activated themselves

2. can respond to non-protein antigens

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13
Q

Why does the T-independent B cell response need two signals for activation?

A

the second co-stimulatory signal helps prevent B cells from being activated against polymers from our own bodies like our DNA

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14
Q

Third way to stimulate B cells

A
  • mitogens
  • can bind to molecules on B cells that happen to be associated with BCRs = clustering!
  • clustering occurs independent of any antigen recognition by the BCR = activation of many B cells = polyclonal = many clones of B cells are activated this way
  • not what we want! some parasites use this to confuse our immune system
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15
Q

Maturation of B cells

A
  1. class switching
  2. somatic hypermutation
  3. career decision
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16
Q

when genes for the BCR undergo mutations that increase the affinity of the BCR for its cognate antigen

A

somatic hypermutation

17
Q

cutting and pasting Hc genes on chromosome 14 leads to changes in …

A

antibody class

18
Q

Like five IgG structures held together by a J chain

A

IgM

19
Q

This antibody is very good at activating the complement classical pathway

A

IgM

  • does this by allowing two C1qrs protein complexes to come together via its Fc region when IgM binds to its cognate antigen on an invader
  • the C1s lose their inhibitor molecule which leads to activation of a C3 convertase
20
Q

This antibody class is a good neutralizer and can cross the placenta and protect a fetus

A

IgG

21
Q

Half life of IgM vs IgG

A

one day vs three weeks

22
Q

The most abundant class of antibody in the blood

A

IgG

23
Q

Subclasses of IgG

A
  • IgG3 fixes complement well, and can be recognized by NK cells (ADCC
  • IgG1 is a great opsonizer and cna enhance phagocytosis
24
Q

Most abundant antibody of all

A

IgA

- rare in blood but very common on mucosal surfaces and in mucosal secretions

25
Q

IgA structure

A

like two IgGs held together by a clip protein

  • clip is a ‘passport’ for secretion into gut
  • also a good neutralizer and found in breast milk
26
Q

T or F. IgA activates complement and can opsonize

A

Doesn’t activate complement and doesn’t opsonize

- Bc otherwise our mucosal membranes will be inflamed all the time!

27
Q

T or F. Mast cells can also phagocytose opsonized bacteria and signal neutrophils to migrate to an infection

A

T

28
Q

Allergies are caused by

A

mast cells degranulating

  • IgE attaches to mast cells Fc receptors after first exposure
  • upon next exposure to allergen, mast cells degranulate releasing histamine, etc.
29
Q

Class switching is controlled by…

A

cytokines produced by Th cells

30
Q

a uniquely high rate of mutation (1000x normal rate) in the V, D, and J region genes after class switching has taken place

A

somatic hypermutation

- affects Fab region of Ab

31
Q

B cell that continues to secrete Ab after migrating to spleen or bone marrow

A

plasma cell

32
Q

This only occurs with T-dependent antigens and Th help

A

Memory B cells