Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

each PROGENITOR B cell can CODE for a distinct antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how B cells recognize antigens

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

2 markers on all MATURE B cells

A

CD19 and CD20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

med involving CD20

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

(EXAM) what B cells recognize specifically

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

are there more BCRs or TCRs and why

A

more BCRs bc takes more diversity to recognize 3D structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

regulatory cytokines IL-10 and TGF-beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

(EXAM) how many potential antibodies for one antigen

A

MANY Abs can recognize the same antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

(EXAM) how many Abs made by one cell

A

ONLY ONE Ab made by a B cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

(EXAM) how many isotypes can an antibody have

A

many. IgM, IgG, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
(EXAM) how B cells approach an antigen + consequence
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.
26
where B cell can be changed so that its Ab becomes better
lymph node. antigen specific B cells undergo affinity maturation
27
how B cells receive Ags in lymph node
through high endothelial venules and lymphoid vessels
28
steps to affinity maturation of B cells
- 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
29
what's somatic mutation of B cells
mutation in areas of their genome called complementarity determining region (for the BCR)
30
how Ags are presented to B cells in the lymph node
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
31
what happens if B cells have a bad interaction with Ag on follicular dendritic cells
they die
32
primary follicle content
Naive B cells who never saw Ag. cells can mature to memory B (go to secondary follicle) or plasma cells
33
secondary follicle content
memory B cells there.
34
how secondary response to an Ag works
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
surface molecules of a regular B cell (meaning other than plasma or memory)
BCR, CD19, CD20, CD40, B7.1, MHC class 2
36
surface molecules of a memory B cell + clinical significance
CD27 on surface. can be used to catch memory cells and grow them to make Abs
37
plasma cells live how long and where | + imp fct other than Ab prod
- many years | - live in plasma cells niches meaning 1. BM or 2. areas of chronic inflammation
38
markers on plasma cell surface
- NO CD19 and CD20**** | - CD38 and CD138
39
significance of plasma cells not having CD20 on their surface
can't use rituximab to treat bad autoimmune disease
40
2 parts of an Ab
- 2 branches of the Y. are the variable part. can twist around, are mobile - stem of the Y = constant region
41
variability in Abs vs TCRs
- TCRs = 10E7 different ones | - Abs = 10E9 diff Abs (diff variable regions)
42
type of molecule Abs are and why + other type of Ab
- glycoproteins. so structure is more mobile. interacts better with Ag and receptor - regulatory Abs exist
43
how Abs recognize Ags vs how they are taken up by phagocytic cells
- with their variable region | - taken up by phagocytic cells via their constant region
44
what forms Ab structure
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
enzyme that cleaves Ab in constant vs variable region
pepsin
46
4 classes of constant regions of Abs (4 classes of heavy chains)
G A M E (D too but only involved in B cell maturation and doesn't circulate)
47
2 possible light chains and normal ratio + significance
kappa and lambda. normally 3K to 1L. | Multiple myeloma = plasma cells make 1 kind so dx it by detecting light chains
48
consequences of B cell dysfunction (which is the most common immune deficiency)
- no abs - moderate to severe bacterial infections (pneumococcus, moraxella, hemophilus influenza, mycoplasma and species, pneumonia, sinusitis, etc)
49
types of humoral immune disorders
- 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
IgM % of circulating Igs + good vs bad
10% good = neutralization (capturing things) and complementation (activate complement) bad = opsonization
51
IgM structure
pentamer. linked by disulfide bonds and a J-chain
52
Why IgM is bad at opsonization
Fcmu (FcM) receptors don't exist (on phagocytic cells. so can't do opsonization which is tagging for phagocytosis)
53
how IgM switches to IgE, IgA or IgG
- gene rearangement | - cytokine and environment dependent process
54
IgG % of circulating Igs + 4 subclasses and %
``` -*****75% of circulating**** IgG1 (70%) IgG2 (20%) IgG3 (5%) IgG4 (5%) ```
55
IgG4 role
regulatory inhibitory Ab
56
(EXAM) Characteristic that is unique to IgG Abs + clinical significance
ONLY ANTIBODY THAT CROSSES THE PLACENTA (mostly in 3rd trimester). premature babies have no IgG.
57
when IgG crosses placenta and stays until when
3rd trimester of pregnancy (premature baby = no IgG). Abs stay in baby until 3-4 months of age
58
(imp) IgG half life after age 3-4 months
21 days (gone after 5 half lives. 120 days)
59
IgG 1 to 4 subtypes: what each is especially good at doing (1.
IgG1: capture bacteria and polysacch IgG2: capture polysacch IgG3: fixing the complement IgG4: regulatory inhibitory Ab
60
physiological naiter def + clinical significance
lowest amount of Abs at 4 months after birth. | must vaccinate early to prime immune resp and protect child
61
cytokines for IgA production
TGF beta and IL-10 (also specific for T reg cells)
62
IgA location and function
- 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
IgA structure and consequence
- dimer (2 molecules + J chain, secretory piece added for protection from proteolysis) * dimer so doesn't bind to phagocytic cells
64
T-B comm. CD28:B7.1. CD40L:CD40. : cytokines that lead to IgG1, IgG2 and IgG3 production
IFN-gamma and IL-4
65
T-B comm. CD28:B7.1. CD40L:CD40. : cytokines that lead to IgA and IgG4 production
IL-10 and TGF-beta
66
T-B comm. CD28:B7.1. CD40L:CD40. : cytokines that lead to IgE production
IL-4 or IL-13 with or without IL-9
67
T-B comm. CD28:B7.1. CD40L:CD40. : cytokines that lead to a very intense activity of plasma cells (all Ig isotypes augmented)
IL-6 and IL-21
68
time for IgA and IgG and IgE formation after B-T interaction
7 days for IgA and IgG. | >7 days for IgE (so no allergy after 1st exposure)
69
time of maximal immune response after B-T interaction and what you developed at that point
21 days. now have plasma cells and memory cells.
70
location of memory cells in the lymph node
secondary follicle (primary is where initial Ag presentation occurs)
71
3 reasons why 2nd resp to same Ag is better
- 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
Fc receptor found where
on phagocytic or cytotoxic cells
73
neutralization def
Ab binds floating Ag
74
opsonization def
Ab binds floating Ag. Ab part of the Ab-Ag complex binds Fc receptor on phagocytic cell. it eats the complex.
75
neutralization is good against which threats
bacteria and toxins
76
IgA is good against which threats
viruses and mycoplasma + clear it out of lungs and gut (bc IgA is mucosal)
77
complement fixation def
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions