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Immunology > B lymphocyte mediated immunity > Flashcards

B lymphocyte mediated immunity Flashcards

1
Q

what are the 2 roles of BCRs

A
  1. initiate signalling cascade upon Ag binding
  2. deliver Ag to intracellular sites for antigen processing & presentation to T-helper cells
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2
Q

what are the 2 types of B cell activation

A

thymus-dependent: via T-helper cells
thymus-independent: via BCR clustering

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3
Q

thymus-dependent B cell activation

A
  • needs the help of T cells
  • presents protein antigens
  • CD40:CD40L is the signal for survival
  • T cell secretes IL-21 for proliferation and differentiation
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4
Q

thymus-independent B cell activation

A
  • 2 types: TI-1 antigen (clustering of BCRs, TLR) TI-2 antigen (BCR + C3d and CR2)
  • BCR clustering leads to signalling
  • presents multivalent antigens (carbohydrates)
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5
Q

what is linked recognition

A

how B cells and T cells work together in B lymphocyte mediated immunity -to mount an immune response against the same pathogen
- present in B cell mediated immunity

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6
Q

what is the second signal required for B-cell activation by thymus-dependent antigens

A
  • from helper TCR:MHC II
  • IKK, P50/p65 and NIK, RelB/p100
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7
Q

what is the second signal required for B-cell activation by thymus-independent antigens

A
  • from TLR
  • myD88 and IKKy
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8
Q

what is the first signal required for B-cell activation

A

PI-3 kinase activates Ras/MAPK

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9
Q

what is Mcl1

A

anti-apoptotic gene which is transcribed in the thymus-dependent pathway of B-cell activation

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10
Q

what are the different signals T-helper cells provide to activate B cells and control their differentiation

A

IL-6
TGF-B
IFN-y
IL-4

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11
Q

how do T-helper cells provided help to B cells that recognize a linked epitope

A
  • T cells are activated to antigens that may reside within the viral particle
  • B cell that recognizes a surface epitope of a virus can process and present other antigen epitopes
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12
Q

how do antigen-binding B cells meet T cells at the border between T-cell area and B-cell follicle in SLO’s
(give step by step)

A
  • before activation resting B cells express CXCR5 and reside in follicles, T cells express CCR7 and reside in T-cell zones
  • activated B cells induce CCR7 and EBI and T cells induce CXCR5
  • both cells migrate to follicular and inter-follicular regions
  • B and T cells aggregate at the periphery of follicles
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13
Q

what is the fate of B and T cells after they aggregate in periphery of follicles

A
  • some B cells migrate to form a primary focus and differentiate into plasmablasts
  • some T cells induce Bcl-6 and become T-FH cells
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14
Q

what are the 2 possible differentiation steps that B cells which receive T cell help can undergo

A
  1. T-FH interaction, remain in follicle: form plasma blast (primary focus) + plasma cell
  2. no T-FH interaction, outside follicle: form germinal center
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15
Q

what is the difference between a primary and secondary focus?

A
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16
Q

when inside lymphoid follicles, activated B cells form…

A

germinal centers

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17
Q

when B cells form germinal centres inside lymphoid follicles, how do the plasma cells get to bone marrow?

A
  • when B cell encounters antigen in the follicle it forms a primary focus
  • some proliferating B cells migrate into the follicle to form a germinal centre
  • plasma cells migrate to the medullary cords or leave via efferent lymphatics
  • plasma cells migrate to the bone marrow
18
Q

what are the different zones of germinal centers

A
  1. mantle zone
  2. Dark zone
  3. Light zone
19
Q

The dark zone of a germinal center

A
  • contains rapid proliferating B cells (centroblasts) that express CXCR4
  • CXCR4 is attracted to CXCL12 produced in dark zone
  • densely packed with proliferating cells
  • somatic hypermutation of Ig genes happens here
20
Q

The light zone of a germinal center

A
  • contains T-FH cells
  • contains slower proliferating B cells (centrocytes) that express CXCR5
  • CXCR5 is attracted to CXCL13 by follicular DCs in light zone
  • affinity maturation where B and T-FH test reactivity to new Ig happens here
  • cells can return to dark zone for additional rounds of Ig mutation if needed
21
Q

which area of the germinal centre does class switching happen in

A

the dark zone

22
Q

centrocyte vs centroblast B-cell make-up

A

centrocyte: CXCR5, CD83, CD86
centroblast: CXCR5, CXCR4

23
Q

where does the primary antibody become diversified

A

centroblasts (dark zone)
includes somatic hypermutation and class switch

24
Q

what is affinity maturation

A
  • IgM is the first antibody made but does not have high affinity
  • somatic hypermutation introduces mutations into the rearranged Ig V regions that improve antigen binding
  • antigen-driven process that generates antigens with higher affinities
  • occurs in light areas
  • relies on T-FH cells
25
Q

basis of class (isotype) switching

A
  • facilitated by cytokines secreted by T-helper cells
  • occurs within the germinal centre AFTER antigen contact
  • class switch from C-u to C-e H chain constant region gene initiated by AID
26
Q

what is AID

A

activation-induced cytidine deaminase
initiates Ig gene rearrangement for class switching

27
Q

which antibodies are produced before class switching

A

IgM and IgD

28
Q

which antibodies are produced after class switching

A

IgA, IgG and IgE

29
Q

IgM isotype characteristics

A
  • Default C region used for mature naive B cell Ig
  • rapid first phase of B cell response to primary infection
  • low affinity
  • large, primarily in blood
30
Q

IgD isotype characteristics

A
  • co-expressed with IgM during maturation
  • no known function
31
Q

IgG isotype characteristics

A
  • class switching
  • 4 subclasses
  • monomeric
  • small, diffuses into tissues
  • found in blood and extracellular fluid
  • the predominant antibody class
  • transported across the placenta
  • high affinity
32
Q

IgE isotype characteristics

A
  • class switching
  • monomeric
  • small, diffuses into epithelial tissues, but less abundant
  • sensation of type 2 immune cells (mast cells)
  • high affinity
33
Q

IgA isotype characteristics

A
  • class switching
  • can exist as monomers or dimers
  • smaller, diffuse into secretions at mucosal epithelial surfaces
  • transferred through breast milk
  • high affinity
34
Q

which antibody classes can diffuse into extravascular sites

A

all IgG classes and the IgA monomer

35
Q

which antibody class transports across the epithelium

A

IgA dimer

36
Q

what are the 5 mechanisms of protection by antibodies

A
  1. neutralization
  2. opsonization
  3. antibody-dependent cell-mediated cytotoxicity by NK cells
  4. sensitization by mast cells
  5. compliment activation
37
Q

protection by antibodies: neutralization

A
  • antibody protects cell by blocking toxin or bacterial adhesion binding to cellular receptors
  • best neutralizers = IgA and IgG
  • neutralizing antibodies function without additional activation of other immune cells
38
Q

protection by antibodies: opsonization

A
  • allows for phagocytosis of the pathogen
  • best opsonins = IgM and IgG
  • mediated by Fcu/y receptors on phagocytes (macrophages and neutrophils)
39
Q

protection by antibodies: antibody-dependent cell-mediated cytotoxicity by NK cells

A
  • NK cells (or CD8 T cells) destroy antibody-bound targets by ADCC
  • best ADCC activation antibodies = IgG
  • antibody binds antigens on the surface of target cells and the Fc receptors on NK cells bind these antibodies to kill cell by apoptosis
40
Q

protection by antibodies: sensitization by mast cells

A
  • best mast cell activating antibody = IgE
  • antigen binding cross-links IgE molecules to activate mast cell and release granule contents
  • also activates anti-parasitic functions
41
Q

protection by antibodies: complement activation

A
  • best complement activators = IgM and IgG
  • C1q binds one IgM OR 2 IgG
  • C1q:CRP’s complex then binds to antibodies binding microbes

Immunology (20 decks)

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