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MICR 3230 > final exam > Flashcards

final exam Flashcards

1
Q

cells in outer cortex of thymus

A

immature proliferating cells

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2
Q

cells in inner cortex of thymus

A

mature cells undergoing selection

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3
Q

double negative (DN) where

A

subscapular zone of cortex

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4
Q

double positive (DP) where

A

inner cortex

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5
Q

single positive (SP) where

A

medulla

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6
Q

3 checkpoints in T-lymphocyte development

A
  1. Pre-TCR (DN3)
  2. Positive Selection (DP)
  3. Negative selection (SP)
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7
Q

where does each checkpoint occur (T-lymph)

A
  1. DN3 (subscapular zone of cortex)
  2. DP (inner cortex)
  3. SP (medulla)
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8
Q

Gene rearrangement in aB T-cells

A

B chain: 4 attempts, 2 clusters of DB and JB segments
a chain: unlimited attempts

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9
Q

what happens after B chain rearrangement stops

A

CD4/CD8 induction, a transcription starts

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10
Q

what rearrangement causes surface expression of aB CD3

A

Va to Ja

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11
Q

what happens at T-lymphocute checkpoint 2

A

Positive selection
- by APC or cTEC
-T-cell that binds self MHC molecule matures
-MHC RESTRICTION

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12
Q

what happens at T-lymphocyte checkpoint 3

A

Negative selection
-mTEC of DC
-remove T cells with TCR w too high affinity to self MHC (apoptosis)
-SELF-TOLERANCE

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13
Q

AIRE

A

displays peripheral antigens, show to T -cells to educate them before leaving thymus
- deficiency = self-reactive T cells

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14
Q

markers in early T-cell development in thymus

A

cKIT: receptor for stem growth receptor
CD44: adhesion molecules
CD25: a chain IL2 receptor

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15
Q

3 fates of developing thymocytes in cortex

A
  1. no bind affinity = death by neglect (apoptosis)
  2. Low/moderate affinity = positive selection/maturation to SP thymocyte
  3. Negative selection/apoptosis
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16
Q

How can a thymocyte leave thymus?

A
  1. right core receptor
  2. right bind affinity
  3. doesnt bind self-antigens
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17
Q

Thymic emigration due to what signalling

A

S1P (high conc in blood and lymph)
- up-regulated by CD4+ and CD8+ (enter medulla 7-14 days, upregulate CD4 and CD8 and leave)

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18
Q

TF that commit to being B cell

A

E2A, FOX01, EBF, PAX

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19
Q

checkpoints in B-lymphocyte maturation

A
  1. Pre-BCR test
  2. Negative selection 1 (central tolerance)
  3. Negative selection (peripheral tolerance)
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20
Q

Checkpoint 1 B-lymphocyte

A

pair w surrogate light chain (kappa5 or VpreB)
-proliferation and progression to L chain rearrangement
-test VDJ recomb of 1 H chain/chromosome
-ALLELIC EXCLUSION
-antigen-independant

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21
Q

Pre B-cell vs pre T-cell

A

Pre B:
- inhibit H chain recomb
-prolif Pre-B cell
-Stim kappa light chain recomb
-shut off surrogatelight chain rec

Pre T:
-Inhib B chain recomb
-Prolif pre-T chain
-stim a chain recomb
-Express CD4 and CD8
-shut off PTa transcription

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22
Q

Checkpoint 2 in B-lymphocyte develop

A

Negative selection 1
- immature B-cell
- CENTRAL TOLERANCE
- if no self-rxn migrate to periphery
-if multivalent molecule receptor editing and apoptosis

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23
Q

Checkpoint 3 in B-lymphocyte development

A

Negative selection 2
- PERIPHERAL TOLERANCE
- transitional B-cell
-BCR that recognize cell molecule can only undergo apoptosis (no editing)

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24
Q

No self-rxn what antibody

A

IgM and IgD

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25
Q

receptor editing

A

L chain rearrange give immature B cells in bone marrow chance to replace autoreactive BCR

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26
Q

Transitional B cells complete maturation in the

A

spleen

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27
Q

Transitional B cells in follicle

A

Enter follicle –> survival signal –> follicular B cell or marginal B cell

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28
Q

Transitional B cells not in follicle

A

Not in follicle –> fail to receive survival signal, die

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29
Q

BAFF on FDC/T1B and T2B

A

Stim BAFF-R on T1B
T1B: increase IgM, no IgD, BAFF-R
T2B: IgM+IgD, CD21

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30
Q

Formation and organization of secondary lymphoid organs by

A

TNF family members

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31
Q

B and T cells enter secondary lymphoid organs via small blood vessels called

A

high-endothelial blood vessels (HEV)

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32
Q

Delivery and migration of B and T cells in the spleen

A
  1. Circulating B and T cells delivered into marginal sinus
    - marginal sinus enriched with marginal zone B cells - do not recirculate)
  2. T cells migrate into T-cell zones (PALS), B-cell to B-cell follicle
    - FRC and FDC
  3. IN spleen antigen delivered via arterioles –> antigen taken up by dendiritc cells, transport antigen to T-cell zone
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33
Q

fibroblast reticular cells (FRC)

A

stromal cells of spleen
- produce chemolines to attract T cells from marginal sinus

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34
Q

follicular dendritic cells (FDC)

A

concentrated in follicles
- produce chemokine CXCL3 to attract B-cells

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35
Q

what attracts T cells into T-cell zones

A

chemokines by FRC

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36
Q

what attracts B cells into follicles

A

CXCL13

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37
Q

MALT

A

mucosa-associated-lymphoid tissue
- peyer’s patch

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38
Q

M cells

A

delivers antigens and pathogens from gut lumen to lymph

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39
Q

Naive T-cell migration into lymph node

A
  1. Circulating lymphnode enters high endothelial venule in lymph node
  2. Binding of L-selectin to GlyCAM-1 and CD34 = rolling interaction
  3. LFA-1 activated by CCr7 signal (in response to CCL21 or CC19) bound to endo surface
  4. Activated LFA-1 tightly bind to CAM-1 –> crosses endothelial enters lymph node via diapedesis
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40
Q

Naive T-cell recirculation through secondary lymph enter and exit from

A

enter: HEV
exit: cortical sinus

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41
Q

Naive T-cell activated by what and what is the process

A

Activated by antigen presentation from DC
-lose ability to exit T-cell, start to proliferate (several days)
-differentiate into effector cells, leave

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42
Q

antigen-specific T-cells recruited/retained where

A

lymph node, trapped in lymph fluid

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43
Q

Local inflammation stimulates (influx/efflux of lymphocyte in lymph node)

A

increase in influx, decrease in efflux

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44
Q

Egress mediated by

A

S1P gradient

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45
Q

S1P gradient

A

-S1P lyase enzyme production by stromal cells in T-zone –> degrade S1P
- no T-cell activation up-regulates S1PR1
-cell sense gradient = egress

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46
Q

S1PR1 and CD69

A

opposite rxn

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47
Q

T-cell activated by antigen (S1PR1 and CD69)

A

T cell activated
-upreg CD69 –> internalize S1PR1 retention
-eventually re-express S1PR1 as CD69 expression decrease –> eress

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48
Q

FTY720

A

cant be inactivated by S1P lyase
-inhibit T-cell egression by down modulating S1PR1 expression

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49
Q

APC in secondary lymph node

A

Dendritic cells
- ubiquitus, throughout body
-Activate naive T cells

Macrophages
-lymphoid & connective tissues, body cavities
-Activation of macrophages by effector and memory cells

B cells:
-lymphoid tissues, peripheral blood
- delivery of help to B cell by TFH cell

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50
Q

Steps of conventional DC in nonlymph to deliver antigens in lymphoid tissues

A
  1. immature conventional DC (in tissue) encounter pathogens, activated by MAMPs
  2. TLR signaling –> CCR7 expression –> enhanced processing of pathogen derived antigens & down regulation of non CCr7 chemokine rec & antigen uptake rec
  3. CCR7 -> direct migration of DC into lymph node: assoc with lower synthesis of new MHC molecules & expression of co-stimulatory molecule
  4. Activated DC in T-cell zone primes naive T-cells
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51
Q

Priming

A

first contact antigen-specific naive T-cells have with antigen

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52
Q

B7

A

on DC: upregulated in case of infection

53
Q

2 types of dendritic cells and differences

A

conventional dendritic cells (cDC)
- activation of naive T cells
- in non-lymphoid tissues

plasmatoid dendritic cells (pDC)
- senses viral infection, secrete interferons
- large amount of type I interferons

54
Q

Type of pathogen, MHC and naive T-cell: Receptor-mediated endocytosis

A

-extracellular bacteria, fungi
-MHC II
-CD4

55
Q

Type of pathogen, MHC and naive T-cell: Macropinocytosis

A

-Extracellular bacteria, soluble antigen, virus
-MHC II
-CD4

56
Q

Type of pathogen, MHC and naive T-cell: viral Infection

A

-virus
-MHC I
-CD8

57
Q

Type of pathogen, MHC and naive T-cell: Cross-presentation after uptake

A

-virus
-MHC I
-CD8

58
Q

Type of pathogen, MHC and naive T-cell: Transfer from DC to resident DC

A

-virus
-Both MHC
-Both T-cells

59
Q

Adhesive interactions between T cell and DC stabilized by specific antigen recognition:

A
  1. T-cell bind APC through lower affinity LFA-1 iCAM-1 interactions
  2. Subsequent binding of T_cell rec –> LFA undergo conformation change
  3. Conformational change = increase affinity and avidity –> prolonged cell-cell contact
60
Q

3 signals in naive T-cell activation by APCs

A
  1. TCR recognize antigen:peptide:MHC on surface of activated cDC
  2. Co-recognition of costimulatory molecule (CD28-B7)
  3. cytokines delivered to activated naive T-cell by APC
61
Q

What drives clonal expansion

A

IL2

62
Q

Initial T-cell response to antigen results in

A

clonal expansion

63
Q

Binding of Il-2 to receptor

A

increase proliferation, affinity
(only on activated T-cells)

64
Q

CTLA4 and clonal expansion

A

Binds 2 B7 dimers, outcompetes CD28 for binding
-can be internalized when bound B7 (remove from APC surface)
-can trasmit negative signal, inhibit T-cell receptor signalling

65
Q

what happens after rapid clonal expansion/ how many days does it take

A

T-cells differentiate into effector cells
-no longer need co-stim to peform cytotoxicity or cytokine secretion

66
Q

Up/down regulation of signals in naive T-cell vs effector

A

Naive:
+TCR
++L-selectin
++CCR7
+LFA-1
+S1PR1
-VLA-4

Effector:
+TCR
-L-selectin
-CCR7
++LFA-1
-S1PR1 (CANT LEAVE)
+VLA-4

67
Q

LFA-1

A

deposit HEV

68
Q

TH1 cells (major cytokines, immune cell types targeted for recruitment, source of antigens targeted)

A

-IFNy (macrophge)

-dead intracellular bacteria

-microbes that resost macrophage killing, extracell bacteria

69
Q

TH2 cells (major cytokines, immune cell types, source of antigens targeted)

A

-IL-4/IL-5 (bone marrow)
-IL-13 (goblet cells)

-eosinophil, mast cell, basophil

-Helminth parasites

70
Q

TH17 cells (major cytokines, immune cell types, source of antigens targeted)

A

-IL-17 (stromal cells)
-IL-22 (epithelial cells)

-neutrophils

-extracellular bacteria/fungi

71
Q

TFH cells (major cytokines, immune cell types, source of antigens targeted)

A

-IL-21 (B-cells)

-B-cell
-plasma cell

-all microbes

72
Q

Treg cells (major cytokines, immune cell types, source of antigens targeted)

A

-TGFB, IL-10 (conventional DC)

-decrease CD4 (lack of T-cell activation)

-self and microbiome derived

73
Q

Cytotoxic T-lymphocyte(CD8+)

A

-bind to virus infected cells
-programs for death
-migrates away from cell
-target cell death by apoptosis without affecting neighbouring cell

74
Q

Cytotoxic effector proteins and their functions

A

Perforin
-aids in delivering contents of granules into cytoplasm of target cell

Granzyme
-serine proteases activate apptosis once in cytoplasm of target cell

Granulysin
-antimicrobial action, induce apoptosis

75
Q

Apoptosis extrinsic pathway

A
  1. trimeric Fas ligand binds and trimerizes Fas
  2. clustering death domains in Fas cytoplasmic domains allows Fas to recruit FADD via its death domain
  3. DED recruit and activate pro-caspase 8
  4. caspase 8 cleaves pro-capase 3 –> cleave I-CAD –> CAD enters nucleus and cleaves DNA
76
Q

Apoptosis intrinsic pathway

A
  1. mitochondria releases cytochrome c (normally only present in mitochondria) –> binds to Apaf-1 induces conform change
  2. Apaf-1:cytochrome complex self-assembles into autosome –> activates millions of copies of pro-caspase 9 –> activate pro-caspase 3
  3. Caspase 3 cleave I-CAD –> release CAD to enter nucleus and cleave DNA
77
Q

Thymus independant antigens

A

TI-1
TI-2
-Multivalent antigen, repeating epitopes (carbs, polysaccharides)
-Facilitate BCR clustering and signaling

78
Q

Thymus dependant antigen

A

TD
-Protein antigens
-Need T-cells
-CD40:CD40L survival and proliferation
-IL-21 prolif and differentiation

79
Q

Second signal for B-cell activation by TD and TI antigens

A

linked recognition

80
Q

CD4 T cell signal to activate B cell and control differentiation

A
  1. antigen recognition by TFH cells that activate B cells
  2. B-cell proliferates –> plasmoblasts –> form primary focus
  3. Further differentiation –> to germinal centre, resting memory cells, antibody-secreting plasma cells
81
Q

CD40:CD40L

A

survival and proliferation

82
Q

IL-21

A

proliferation and differentiation

83
Q

Cytokines in B cell activaition role

A

isotype switching

84
Q

linked recognition

A

T-cell: activated to antigens residing in viral particle

B-cell: recognizes surface epitope of virus

Both: TFH cell provides help to B cells that recognized linked epitope

85
Q

without recognition

A

BCR takes up processes antigen without help from T-cell

86
Q

Antigen bind B-cells meet T-cells where

A

between T cell area and B-cell follical in SLO

87
Q

Not activated vs activated B cells and T cells (resting vs migration)

A

Not activated:
B: in follicles, CXCR5
T: in T-cell zones, CCR7

Activated:
B: induce CCR7 and EB12
T: induce CXCR5
migrate

B & T cells –> aggregsate at periphery of follicles

B cells (some) –> migrate to form primary focus
T cells (some) –> induce Bcl-6 and become TFH

88
Q

BAFF

A

survival signal for B cells

89
Q

B cell (mature) in vs out of follicle

A

out: no TFH –> plasmablast –> memory
(first phase)

in: germinal centre secondary lymph —> memory plasma cell
(second phase)

90
Q

Activated B cells from germinal centers

A
  1. naive B cells travel to lymph node via bloodstream leave via efferent lymph
  2. encounter antigen in follicle, form primary focus –> some proliferating B cells migrateinto follicle to form germinal center
  3. plasma cells migrate to medullary cords or leave via efferent lymphatics
  4. plasma cells migrate to bone marrow
91
Q

3 germinal center zones

A
  1. mantle zone
  2. dark zone
  3. light zone
92
Q

mantle zone of germinal center

A

-peripheral edge of follicle
-contain resting B cells

93
Q

dark zone of germinal center

A

-rapidly prolferating B cells that express CXCR4 –> attracted to CXCL12 in dark zone
-densely packed reg of proliferating cells
-Ig mutated
SOMATIC HYPERMUTATION

94
Q

light zone of germinal center

A

-contain TFH cells
-slow proliferating B cells (centrocytes) that lose CXCR4 and express CXCR5 –> attracted to CXCL13 by FDCs
-B cells undergo Ig mutation and interact w TFH to test reactivity to new Ig
-can return to dark zone for maturation
-AFFINITY MATURATION

95
Q

reentry into dark zone (for maturation) depends on

A

CXCR5 re-expression

96
Q

when does affinity maturation occur and what does it do

A

-after somatic hypermutation and class switching
-mutation to rearrange Ig V regions
-generate antibodies with higher affinity
-antigendriven occur in germinal center

97
Q

Antibody functional activity: Neutralization

A

IgG and IgA
-block binding of toxins
-block bacterial adhesion binding

98
Q

Antibody functional activity: Opsonization

A

IgM and IgG
-aggregation of IG on bacterial surface cause cross-link of Fc receptors
-activation of macrophage = phagocytosis
-mediated by Fcu/y rec on phagocytes

99
Q

Antibody functional activity: Sensitization for killing by NK cells

A

IgG
-Fc receptor on NK recognize bound antibody
-cross-linking of Fc cause NK to kill target cell
-antibody-dependant cell-mediated cytotoxicity (ADCC)

100
Q

Antibody functional activity: Sensitization of mast cells

A

IgE
- resting mast: granules contain histamine etc
-antigen cross-links bound IgE: release granule content

101
Q

Antibody functional activity: Activate complement system

A

IgG and IgM

IgG: bind antigen –> C1q binds at least 2 Ig –> activate C1r –> cleave/activates C1 serine proteases

IgM: (pentamer) vinds antigen –> C1q bind antigen –> C1q bind IgM (1)

102
Q

Phases of course of infection

A
  1. establishment of infection
    - pathogen produces PAMPS
  2. inductive phase
    - adaptive
    -cytokine, chemokines educate, virus takes control
  3. effector phase
    - majority of adaptive, lower microorganism
  4. memory phase
    - T and B cells remember pathogen
103
Q

Primary immune response

A

first time seeing pathogen

104
Q

Secondary immune response

A

second time seeing pathogen

105
Q

Progression of infection (innate to adaptive)

A
  1. Local infection, penetration of epithelium
    -INNATE: bacteria taken up
    -macrophage, chemokines, cytokines
    -neutrophils, NK cells, dendritic cells
    (take up antigen, migrate to seocondary lymph)
    -complement
  2. Local infection of tissues
    - dendritic cells migrate to secndary lymph
    -same as above
  3. Lymphatic spread
    -pathogens trapped/ phagocytosed in lymph tissue
    -migrating DC initiates adaptive immunity
  4. Adaptive
    -T-cell helps innate
106
Q

groups of ILCs

A

Cytotoxic T-cells
- virus
- IL-12, IL-15 –> NK –> IFN y

Group 1 ILC
- intracellular bacteria
- IL-12 –> Il-18 –> ILC1 –> IFN y

Group 2 ILC
- parasites
-tuft cells –> TSLP, IL-25, IL-33 –> ILC2
–> IL-13 & IL-15 (also eosinophils, mast cells, basophils)

Group 3 ILC
- Extracellular bacteria
-IL-23 & IL-1B –> ILC3 –> Il-17 & IL-22

107
Q

TH1

A

Type 1 T-helper cell
-virus/intracell
-Tbet - IFNy –> macrophage
-ILC1

108
Q

TH2

A

Type 2 T-helper cell
-parasites
-eosinophils/mast cells/basophils
-ILC2

109
Q

TH3

A

Type 3 T-helper cell
-extracellular bacteria
-neutrophil (help phagocytose)
-ILC3

110
Q

primary immune response includes

A

T & B cell activation, differentiation and proliferation

111
Q

Primary vs. secondary immune response: type of B cell

A

Primary: naive
Secondary: memory

112
Q

Primary vs. secondary immune response: lag time

A

Primary: 4-7 days
Secondary: 1-3 days

113
Q

Primary vs. secondary immune response: time of peak response

A

Primary: 7-10 days
Secondary: 3-5 days

114
Q

Primary vs. secondary immune response: magnitude of peak response

A

Primary: depends
Secondary: 100-1000x higher

115
Q

Primary vs. secondary immune response: isotype

A

Primary: IgM
Secondary: IgG

116
Q

Primary vs. secondary immune response: antibody affinity

A

Primary: lower
Secondary: higher

117
Q

Models of memory T-cell development

A
  1. Linear model
    -memory T-cells arise from effector T-cells as primary immune response subsides
  2. Branching model
    -antigen-activated naive T cells give rise to daughter cell that commits to either effector or memory
118
Q

smallpox eradicated in

A

1980

119
Q

central vs effector memory cell

A

central: express CD62L and CCR7, circulate through lymph tissue

effector: lack, migrate to nonlymph

120
Q

CD62L

A

selectin for migration to lymph nodes

121
Q

CCR7

A

chemokine receptor, help move to lymph nodes
-naive, TCM

122
Q

CD45RA

A

marker for naive, in lymph nodes, Treceptor signal

123
Q

CD45RO

A

marker for memory effector T cells

124
Q

BCl-2

A

prevents apoptosis, survival signal
-TCM,TEM,TRM,naive

125
Q

Migratory patterns of each memory T-cell

A

Naive: efferent lymph, CCR7, passes T-cell zone

TCM: blood, T-cell zone of SLO and lymph

TEM: everywhere
-nonlymph: lymph, lymphnodes, blood
-some remain in blood circulation, migrate through spleen

TRM: dont recirculate, confined to 1 tissue

126
Q

Long-term survival of memory T-cells depends on

A

IL-7 and IL-15

127
Q

Naive T-cell needs what to survive

A

need survival signal and contact with self-peptide:self MHC complexes to survive

128
Q

What happens when naive encounter antigen

A

most become effector cells –> some become long-lie memory cells –> need IL-17

129
Q
A

MICR 3230 (4 decks)

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