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Bloc F - Defense > Mar21 M3-Adaptive Immunity 2 > Flashcards

Mar21 M3-Adaptive Immunity 2 Flashcards

1
Q

(EXAM) B lymphocytes % of circulating lymphocytes

A

5-15%

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2
Q

(EXAM) how diverse is the recognition of antigens by B cells

A

each PROGENITOR B cell can CODE for a distinct antigen

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3
Q

how B cells recognize antigens

A

BCRs (B cell receptor) on surface (looks like an Ig so called surface Ig)

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4
Q

after B cells recognize antigens with they BCR what do they do

A

act like APC. eat the antigen and present it on MHC class 2 to T cells

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5
Q

2 markers on all MATURE B cells

A

CD19 and CD20

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6
Q

med involving CD20

A

rituximab, a CD20 Ab. binds B cells so they’re eliminated in the spleen. (cancers + autoimmune diseases)

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7
Q

immature or naive B cell def

A
  • *The B cells that come out of the bone marrow and that are released in circulation.
  • secrete BCR that has same isotype as an IgM Ab
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8
Q

how B cells mature

A
  • antigen dependent maturation in the lymph nodes and spleen

- interact with T cells and specialized follicular dendritic cells

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9
Q

(EXAM) what B cells recognize specifically

A

3D structures of antigens (so said to recognize native antigens)

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10
Q

are there more BCRs or TCRs and why

A

more BCRs bc takes more diversity to recognize 3D structures

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11
Q

principle of conjugated vaccine

A
  • conjugated pneumococcal cell wall to piece of diphtheria or tetanus in the vaccine
  • B cell can recognize construct bc sees 3D polysacch cell wall
  • T cell sees a protein so stimulates B cell to make lot of Abs (which will in fact be against pneumococcal polysacch cell wall)
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12
Q

why need to make conjugated vaccine against pneumococcus (why vaccine with pneumococcal cell wall is inefficient)

A
  • No peptides for T cell to recognize (only 3D polysacch wall the B cell can see)
  • T cell won’t produce cytokines to make B cell make a lot of Abs
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13
Q

B cell (AS AN APC) - T cell interaction step 1

A
  • MHC class 2 interacts with CD4

- MHC class 2+peptide interacts with TCR and CD3

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14
Q

B cell (AS AN APC) - T cell interaction step 2 (what happens after antigen presentation)

A
  • T cell secretes cytokines (IFN-gamma and IL-2. note: cytokines of th1 resp to IC organism)
  • T cell upregulates IL-2 receptor and CD40 ligand
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15
Q

why T cell upregulates CD40 ligand within 48 hours

A

will bind adhesion molecule CD40 on surface of B cells to allow talk between B and T cells to make B cells produce antibodies

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16
Q

costimulation molecules (molecules to make closer contact and better activation) in B cell (as APC) - T cell interaction

A
  • B cell has adhesion molecules CD80 and CD86, like dendritic cells
  • stick to CD28 adhesion molecule on T cell
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17
Q

molecules needed for T cell to stimulate B cells (so they make abs)

A
  • CD40 on B cell and CD40L on T cells

- B7.1 on B cells and CD28 on T cells for more ligation and communication

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18
Q

what happens if T cell and B cell don’t touch (for B cell stim). + specific case of dysfunctional CD40L

A
  • B cells only make IgM

- CD40L (on T cells) problem = hyper IgM syndrome

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19
Q

cytokines the T cell uses to make the B cell make IgA

A

regulatory cytokines IL-10 and TGF-beta

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20
Q

cytokines the T cell uses to make the B cell make IgG

A
  • IFN-gamma

- IL-4 OR IL-13 (depending on antigen) will make B cell make a ton of IgG

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21
Q

cytokines the T cell uses to make the B cell make IgE for parasite defense and allergy

A

IL-4 and IL-13

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22
Q

(EXAM) how many potential antibodies for one antigen

A

MANY Abs can recognize the same antigen

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23
Q

(EXAM) how many Abs made by one cell

A

ONLY ONE Ab made by a B cell

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24
Q

(EXAM) how many isotypes can an antibody have

A

many. IgM, IgG, etc.

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25
Q

(EXAM) how B cells approach an antigen + consequence

A

because the antigen is in 3D, different B cells can recognize different 3D pieces.
**can end up making Abs against any part of the protein, lipoprotein, wtv.

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26
Q

where B cell can be changed so that its Ab becomes better

A

lymph node. antigen specific B cells undergo affinity maturation

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27
Q

how B cells receive Ags in lymph node

A

through high endothelial venules and lymphoid vessels

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28
Q

steps to affinity maturation of B cells

A
  • B cells that recognize antigen proliferate and do SOMATIC MUTATION
  • clones that recognize Ag better remain AND BECOME THE MATURE B CELLS (other ones = apoptosis)
  • these clones will form the memory cells for next time
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29
Q

what’s somatic mutation of B cells

A

mutation in areas of their genome called complementarity determining region (for the BCR)

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30
Q

how Ags are presented to B cells in the lymph node

A

follicular dendritic cells (*living in follicles) trap Ags but DON’T process them. hang them on their surface through the complement. B cells interact with the 3D structure

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31
Q

what happens if B cells have a bad interaction with Ag on follicular dendritic cells

A

they die

32
Q

primary follicle content

A

Naive B cells who never saw Ag. cells can mature to memory B (go to secondary follicle) or plasma cells

33
Q

secondary follicle content

A

memory B cells there.

34
Q

how secondary response to an Ag works

A

memory B cells in secondary follicle grab Ag. talk to T cells. T cells talk back to stim them. LOT of memory cells and plasma cells made.

35
Q

surface molecules of a regular B cell (meaning other than plasma or memory)

A

BCR, CD19, CD20, CD40, B7.1, MHC class 2

36
Q

surface molecules of a memory B cell + clinical significance

A

CD27 on surface. can be used to catch memory cells and grow them to make Abs

37
Q

plasma cells live how long and where

+ imp fct other than Ab prod

A
  • many years

- live in plasma cells niches meaning 1. BM or 2. areas of chronic inflammation

38
Q

markers on plasma cell surface

A
  • NO CD19 and CD20**

- CD38 and CD138

39
Q

significance of plasma cells not having CD20 on their surface

A

can’t use rituximab to treat bad autoimmune disease

40
Q

2 parts of an Ab

A
  • 2 branches of the Y. are the variable part. can twist around, are mobile
  • stem of the Y = constant region
41
Q

variability in Abs vs TCRs

A
  • TCRs = 10E7 different ones

- Abs = 10E9 diff Abs (diff variable regions)

42
Q

type of molecule Abs are and why + other type of Ab

A
  • glycoproteins. so structure is more mobile. interacts better with Ag and receptor
  • regulatory Abs exist
43
Q

how Abs recognize Ags vs how they are taken up by phagocytic cells

A
  • with their variable region

- taken up by phagocytic cells via their constant region

44
Q

what forms Ab structure

A

2 heavy chains and 2 light chains.

  • constant region = base of the 2 heavy chains
  • variable region = 2 light chains + 2 branches of the heavy chains
45
Q

enzyme that cleaves Ab in constant vs variable region

A

pepsin

46
Q

4 classes of constant regions of Abs (4 classes of heavy chains)

A

G A M E (D too but only involved in B cell maturation and doesn’t circulate)

47
Q

2 possible light chains and normal ratio + significance

A

kappa and lambda. normally 3K to 1L.

Multiple myeloma = plasma cells make 1 kind so dx it by detecting light chains

48
Q

consequences of B cell dysfunction (which is the most common immune deficiency)

A
  • no abs
  • moderate to severe bacterial infections (pneumococcus, moraxella, hemophilus influenza, mycoplasma and species, pneumonia, sinusitis, etc)
49
Q

types of humoral immune disorders

A
  • No B cells (X-linked agammaglobulinemia)
  • Missing cell comm molecules (hyper IgM syndrome, where CD40L of T cells not working)
  • other poor B or T cell fct diseases (combined immune deficiency, common variable immune deficiency)
50
Q

IgM % of circulating Igs + good vs bad

A

10%
good = neutralization (capturing things) and complementation (activate complement)
bad = opsonization

51
Q

IgM structure

A

pentamer. linked by disulfide bonds and a J-chain

52
Q

Why IgM is bad at opsonization

A

Fcmu (FcM) receptors don’t exist (on phagocytic cells. so can’t do opsonization which is tagging for phagocytosis)

53
Q

how IgM switches to IgE, IgA or IgG

A
  • gene rearangement

- cytokine and environment dependent process

54
Q

IgG % of circulating Igs + 4 subclasses and %

A 
-*****75% of circulating****
IgG1 (70%)
IgG2 (20%)
IgG3 (5%)
IgG4 (5%)
55
Q

IgG4 role

A

regulatory inhibitory Ab

56
Q

(EXAM) Characteristic that is unique to IgG Abs + clinical significance

A

ONLY ANTIBODY THAT CROSSES THE PLACENTA (mostly in 3rd trimester). premature babies have no IgG.

57
Q

when IgG crosses placenta and stays until when

A

3rd trimester of pregnancy (premature baby = no IgG). Abs stay in baby until 3-4 months of age

58
Q

(imp) IgG half life after age 3-4 months

A

21 days (gone after 5 half lives. 120 days)

59
Q

IgG 1 to 4 subtypes: what each is especially good at doing (1.

A

IgG1: capture bacteria and polysacch
IgG2: capture polysacch
IgG3: fixing the complement
IgG4: regulatory inhibitory Ab

60
Q

physiological naiter def + clinical significance

A

lowest amount of Abs at 4 months after birth.

must vaccinate early to prime immune resp and protect child

61
Q

cytokines for IgA production

A

TGF beta and IL-10 (also specific for T reg cells)

62
Q

IgA location and function

A
  • mucosa
  • captures stuff only (no complement act. no osp.) so acts for NEUTRALIZATION (immune response regulator bc of these things it doesn’t do)
63
Q

IgA structure and consequence

A
  • dimer (2 molecules + J chain, secretory piece added for protection from proteolysis)
  • dimer so doesn’t bind to phagocytic cells
64
Q

T-B comm. CD28:B7.1. CD40L:CD40. : cytokines that lead to IgG1, IgG2 and IgG3 production

A

IFN-gamma and IL-4

65
Q

T-B comm. CD28:B7.1. CD40L:CD40. : cytokines that lead to IgA and IgG4 production

A

IL-10 and TGF-beta

66
Q

T-B comm. CD28:B7.1. CD40L:CD40. : cytokines that lead to IgE production

A

IL-4 or IL-13 with or without IL-9

67
Q

T-B comm. CD28:B7.1. CD40L:CD40. : cytokines that lead to a very intense activity of plasma cells (all Ig isotypes augmented)

A

IL-6 and IL-21

68
Q

time for IgA and IgG and IgE formation after B-T interaction

A

7 days for IgA and IgG.

>7 days for IgE (so no allergy after 1st exposure)

69
Q

time of maximal immune response after B-T interaction and what you developed at that point

A

21 days. now have plasma cells and memory cells.

70
Q

location of memory cells in the lymph node

A

secondary follicle (primary is where initial Ag presentation occurs)

71
Q

3 reasons why 2nd resp to same Ag is better

A
  • IgG in 3-5 days, not 7
  • preexisting Abs on previous plasma cells
  • IgM cells (naive) can start a ‘‘new’’ response and make new B cells (memory cells will be less or more sophisticated)
72
Q

Fc receptor found where

A

on phagocytic or cytotoxic cells

73
Q

neutralization def

A

Ab binds floating Ag

74
Q

opsonization def

A

Ab binds floating Ag. Ab part of the Ab-Ag complex binds Fc receptor on phagocytic cell. it eats the complex.

75
Q

neutralization is good against which threats

A

bacteria and toxins

76
Q

IgA is good against which threats

A

viruses and mycoplasma + clear it out of lungs and gut (bc IgA is mucosal)

77
Q

complement fixation def

A

C1q fixes one of its legs to the Ab part of the Ab-bacteria (Ag) complex. complement forms. bacteria lyses.

Bloc F - Defense (57 decks)

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