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micr 386 > module 06 section 02 (B-cell activation) > Flashcards

module 06 section 02 (B-cell activation) Flashcards

1
Q

after mature B-cells exit the bone marrow, what occurs in the periphery in response to an antigen?

A

activation, proliferation, and differentation

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2
Q

most antigens are dependent on what?

A

thymus-dependent - meaning they require direct contact with helper T-cells to activate B-cells

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3
Q

are there thymus-independent antigens?

A

yes - antibody production can also be induced without helper T-cell activity by thymus-independent antigens

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4
Q

observations in mice and humans born without a thymus lead to what discovery?

A

that there are two routes of antibody production following B-cell activation (depending on the nature of the antigen)

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5
Q

explain the T-cell dependent B-cell activation process

A

when a helper T-cell recognizes an antigen:MHC class II complex on a B-cell, the T-cell becomes activated, which activates the B-cell

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6
Q

what are the signals involved in T-cell dependent B-cell activation?

A
  1. TCR-MHC class II complex binding
  2. co-stimulatory molecule signalling
  3. cytokine signalling
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7
Q

describe signal 1 part 1

A
  • requires antigen processing and presentation to T-cells
  • BCR binds its specific antigen resulting in internalization of the Ig-antigen complex by receptor-mediated endocytosis
  • antigen is then processed by the endocytic antigen processing pathway and is displayed on MHC class II molecules on the cell surface
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8
Q

describe signal 1 part 2

A
  • TCR of the helper T-cell recognizes the processed Ag:MHC complex presented by the B-cell
  • TCR and CD4 bind to the Ag:MHC class II complex
  • results in activation of the helper T-cell and completion of signal 1
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9
Q

describe signal 2 part 1

A
  • upon TCR recognition of the antigen, CD40L expression is induced on the surface of helper T-cell through TCR-mediated inositol lipid hydrolysis
  • CD40L interacts with constitutively (always) expressed CD40 on the B-cell
  • CD40L-CD40 interaction activates cytokine receptor expression on the cell surface of both B-cell and T-cell
  • i.e. costimulatory molecule interaction btwn T-cell and B-cell
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10
Q

what is inositol lipid hydrolysis?

A

PIP2 (inositol lipids) on the cell membrane is hyrolyzed

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11
Q

describe signal 2 part 2

A
  • MHC class II mediated cAMP activation results in increased expression of B7 on the B-cell surface
  • B7 binds CD28 expressed by T-cell and provides necessary costimulatory signal to activate the helper T-cell
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12
Q

describe signal 3

A
  • B7-CD28 interaction induces the MAPK cascade in helper T-cells
  • this cascade activates cJUN and cFos which collectively form the AP-1 transcription factor that induces the activation of the IL-2 gene
  • cytokines bind their respective receptors on B-cells and T-cells, initating the proliferation and differentiation phases
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13
Q

what is the mechanism for cytokine secretion used in signal 3?

A
  1. TCR:MHC, CD40L:CD40 and LFA-1:ICAM-1 interactions btwn helper T-cell/B-cell maintains cell-cell contact - contact promotes talin mobilization towards the point of cell-cell contact (without these interactions talin’s localized to cytoplasm)
  2. helper T-cell reorganizes its cytoskeleton towards the B-cell, MTOC, the golgi apparatus and talin are rearranged so that cytokines can be released close to the point of contact btwn T and B cells
  3. the T-cell secretes IaL-4 directly towards the B-cell at the point of cell-cell contact
    - IL-4 promotes B-cell activation, proliferation and differentiation
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14
Q

what is talin?

A

cytoskeletal protein concentrated at all cell-cell contact points in lymphocytes

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15
Q

what is MTOC?

A

microtubule-organizing center - where microtubule skeleton proteins are produced

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16
Q

what are the two potential outcomes for the B-cell upon activation by the T-cell?

A

proliferation or differentation

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17
Q

how does B-cell proliferation result after B-cell activation?

A
  • activated b-cell can undergo proliferation by entering the G1 cell cycle
  • this B-cell proliferation occurs following an additional: IL-1 co-stimulatory signal from activated macrophages and IL-2, IL-4 and IL-5 signals from helper T-cells, to promote the rapid clonal expansion of B-cells
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18
Q

how does B-cell differentiation result after B-cell activation?

A

-cytokines released by helper T-cells cause B-cell differentation by inducing Ig class switching

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19
Q

what type of class switching does IFN-y promote? (also STAT1)

A

to IgG

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20
Q

what type of class switching do IL-5 or TGF-B* promote?

A

to IgA

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21
Q

what type of class switching do IL-4*, IL-5, or IL-13 promote? (also STAT6)

A

to IgE

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22
Q

what type of class switching do IL-4, IL-2 or IL-5 promote?

A

maintain IgM production

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23
Q

recall: what are the principal effector functions of IgM, IgG, IgE and IgA?

A

IgM: complement activator
IgG: Fc receptor-dependent phagocyte responses, complement activation, neonatal immunity
IgE: mast cell degranulation
IgA: mucosal immunity

24
Q

what are cytokine sources?

A

activated CD4 helper T-cells or other activated APCs (macrophages and dendritic cells)

25
Q

recap: list 4 important characteristics of CD40L

A
  • induced by inositol lipid hydrolysis
  • is inducible
  • its expressed on the T-cell surface
  • its interaction with CD40 (on B-cells) activates cytokine receptors
26
Q

describe HIGM syndrome

A
  • X-linked hyper IgM syndrome
  • condition that occurs when there’s a defect/deficiency in CD40L on helper T-cells
  • recessive, X-linked inherited disease (bc CD40L is made by gene on X-chromosome)
  • lack of CD40L results in T-cells that are incapable of inducing class switching
27
Q

what is the result of HIGM in terms of Ig levels?

A

low IgG and IgA but abnormally high IgM in circulation

28
Q

what is the result of HIGM in terms of the patients health?

A
  • patients have defective immunity and are susceptible to various infections
  • patients will experience frequent infections
  • patients may be at greater risk for developing autoimmune disorders, neuological complications, liver disease and GI tumors
29
Q

do helper T-cells engage in the destruction of the virus?

A

no - responsible for sending instructions to all groups of cells engaged in the immune response (engaged in destruction of the virus)

30
Q

what specifically causes fever in response to a viral infection?

A

macrophages present the antigen to the helper T-cells and then secrete fever-inducing hormones (cytokines)

31
Q

what does fever in response to viral infection lead to? (2)

A
  • the creation of a hostile environment for the virus (slows spread)
  • the stimulation of helper T-cell activation
32
Q

what recruits macrophages to the site of infection?

A

the infected cell releases interferon

33
Q

the majority of type 1 T-cell independent (TI-1) antigens are:

A

polyclonal B-cell activators - capable of activating B-cells regardless of their antigenic specificity

34
Q

what does polyclonal mean in terms of the binding the TI-1 antigen?

A

stimulates the proliferation of multiple clones of B-cells into antibody producing cells that are independent of the TI-1 antigenic stimuli, but specific to that B-cell

35
Q

some bacterial cell wall components, including LPS, function as TI-1 antigens, true or false?

36
Q

LPS can interact with:

A
  • TLR4 - present on all B-cells

- BCR - few B-cell populations have LPS-specific BCRs

37
Q

upon TI-1 binding to the receptor, what directs activation, proliferation and differentation of the B-cell?

A
  • protein kinase C signalling pathway

- important in some early stages of infection by extracellular pathogens as its rapidly activated

38
Q

where are type 2 TI antigens expressed?

A

on the surface of pathogens in an organized and highly repetitive form

39
Q

how can TI-2 antigens activate B-cells?

A

by extensively cross-linking the membrane bound Ig in a multivalent fashion

40
Q

what does TI-2 antigen bidning lead to?

A

accumulation of BCR cross activation to evoke antigen specific responses

41
Q

provide examples of TI-2 antigens (2)

A

polymeric proteins or bacterial cell wall polysaccarides (dextrans, flagellin) with repeating polysaccaride units

42
Q

are TI-2 antigens polyclonal B-cell activators?

43
Q

does the B-cell response to TI-2 antigens require direct involvement of helper T-cells?

44
Q

what is required for TI-2 antigens to stimulate efficient B-cell proliferation or to stimulate class switching to isotypes other than IgM?

A

cytokines derived from helper T-cells

45
Q

upon TI-2 binding to the receptor, what directs activation, proliferation and differentation of the B-cell?

A

the inositol lipid hydrolysis signalling pathway

46
Q

which type(s) of B-cell activation require(s) direct contact with helper T-cells?

A

T-cell-dependent antigen

47
Q

which type(s) of B-cell activation require(s) helper T-cell derived cytokines?

A

T-cell-dependent antigen

48
Q

which type(s) of B-cell activation activates mature B-cells

A

T-cell-dependent antigen, T-cell-independent antigen type 1, and T-cell-independent antigen type 2

49
Q

lipopolysaccarides are an example of which type of antigen group?

A

TI-1 antigen

50
Q

flagellin (polymeric proteins) is an example of which type of antigen group?

A

TI-2 antigen

51
Q

albumin is an example of which type of antigen group?

A

t-dependent antigen

52
Q

Igs are an example of which type of antigen group?

A

t-dependent antigen

53
Q

dextran (repeating polysaccaride units on bacterial cell wall) is an example of which type of antigen group?

54
Q

bacterial DNA (binds TLR) is an example of which type of antigen group?

55
Q

TI type 1 antigens are all of the following EXCEPT:

a) involve the activation of the mitogen receptor on B-cells
b) involve no Th cells for activation
c) generate few (if any) antibodies of the IgG isotype
d) generate mainly low affinity antibodies of the IgM isotype
e) involve extensive cross-linking of membrane Igs on B-cells

56
Q

recap: what is the subclassification of T-cell independent antigens based on?

A

type 1: polyclonal B-cell activation

type 2: multivalent receptor crosslinking

micr 386 (31 decks)

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