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DMD 5244 (Immunity) > T-cell development (complete) > Flashcards

T-cell development (complete) Flashcards

1
Q

where does very early thymocyte development occur

A

in the bone marrow

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2
Q

where does final thymocyte development occur

A

in the thymus

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3
Q

what are the steps of thymocyte development in the thymus

A
  1. Double negative
  2. Double positive
  3. Positive/Negative selection to become single positive
  4. final screening to remove autoreactive cells
  5. release into blood stream
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4
Q

When cells arrive at the thymus they aren’t technically T-cells until what

A

a receptor on the cells known as Notch commits them to the T cell lineage

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5
Q

What is the transcription factor that become active when a T-cell is activated by Notch

A

GATA-3

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6
Q

What are the T-cell analogs for the B-cell heavy chain and light chain

A

Alpha chain = light chain

Beta chain = heavy chain

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7
Q

Most T-cells have alpha-Beta TCR’s, what is the other type of TCR that some T-cells have

A

gamma-delta

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8
Q

does allelic exclusion occur in TCR expression, like it does in the Ig expression of B-cells

A

yes, only one of each allele is used in the TCR

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9
Q

The first step of T-cell development is the Double Negative stage, what happens in the development of the TCR in that stage?

A

they undergo Beta selection (creating the Beta chain). then it binds to pre-Talpha chain (just holds the place for the future alpha chain (now it is a double positive thymocyte)

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10
Q

what defines a double negative Thymocyte

A

it has no CD4 or CD8

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11
Q

what defines a double positive thymocyte

A

it has both CD4 and CD8

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12
Q

once a thymocyte has gone through Beta selection and has a pre-T alpha chain, what happens next

A

they are at the Double positive stage of development, and a functional TCR alpha chain replaces the pre-TCR alpha

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13
Q

most thymocytes are in the double positive stage of development. They undergo positive and negative selection. what is positive selection

A

positive selection is testing to see how tightly a T-cell binds self MHC molecules.
they fail if they don’t bind at all (they are supposed to loosely bind)

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14
Q

what is negative selection (central tolerance) of T-cells

A

testing to see how tightly you bind self MHC. to ensure self tolerance.
they fail if they bind too tightly (they are killed)

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15
Q

what happens to T-cells that don’t bind self MHC, and what happens to T-cells that bind self MHC too tightly

A

the cells that don’t bind at all die of neglect (anergy?)

the cells that bind too tightly are killed (apoptosis?)

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16
Q

what does the TCR also bind to when it binds to an MHC class 2 in the transition from a double positive cell to a single positive cell

A

when it binds to the MHC class 2 it also binds with the CD4 molecule, making it a CD4+ T-cell (Helper)

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17
Q

what does the TCR bind to when it binds to an MHC class 1 in the transition from a double positive cell to a single positive cell

A

when it binds to the MHC class 1 it also binds to the CD8 molecule, making it a CD8+ cell (cytotoxic)

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18
Q

what do you call a thymocyte that have just exited the thymus

A

Recent thymic emigrants (RTEs)

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19
Q

what are the main differences between the two types of cell death, Necrosis and apoptosis

A

apoptosis is planned cell death, and doesn’t induce inflammation
Necrosis isn’t planned, and does induce inflammation

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20
Q

what do you always find with apoptosis, regardless of the stimuli that causes it

A

caspases

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21
Q

what are the two types of caspases

A

initiator caspases and effector caspases

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22
Q

what do initiator caspases do

A

they are activated by the death stimulus and activate the effector caspases

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23
Q

what do effector caspases do

A
  1. cleave critical targets necessary for cell survival

2. activate other enzymes that dismantle the cell

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24
Q

what is required for T-cells to become activated

A
  1. antigen presentation
  2. a costimulatory ligands
    They need two signals, and the antigen is the first signal
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25
Q

what happens once a T-cell becomes active

A

they differentiate into their effector forms (CD8+ = cytotoxic cell, CD4+ = other cells)

26
Q

what makes a cSMAC (central supramolecular activating complex)

A

TCR/MHC-peptide complexes and coreceptors

27
Q

what makes a pSMAC (peripheral supramolecular activating complex)

A

adhesion molecules/bound ligands

28
Q

after the T-cell has had its first signal (antigen) and its second signal (costimulatory ligand) does it receive more signals? If yes, what? and what does it cause?

A

Yes
They are cytokines (IL-2, IL-12)
they direct T-cells to differentiate into distinct effector cell types

29
Q

are all costimulatory signals activating (for T-cells)

A

no, there are some that are activating (positive), there are some that are negative

30
Q

what are examples of positive costimulatory signals

A

CD28, and ICOS

31
Q

what are examples of negative costimulatory signals

A

CTLA-4, PD-1, and BTLA

32
Q

where is CD28 found, and what does it bind to

A

it is found on the majority of T-cells, and it binds to B7-1 and B7-2 on APCs

33
Q

Where is ICOS found, and what does it bind to

A

it is found on memory and effector T-cells, and it binds the ICOS-ligand on APCs

34
Q

Where is CTLA-4 found, and what does it bind to

A

it is found on the T-cells and binds B7-1 and B7-2

35
Q

which has a higher affinity for the B7-1 and B7-2 on APCs, CD28 and CTLA-4

A

CTLA-4 (this shuts down the activation)

36
Q

what does PD-1 (the negative costimulator) stand for

A

program death

37
Q

what does BTLA ( the negative costimulator) stand for

A

B and T lymphocytes attenuator

38
Q

what happens to T-cells if they don’t receive their second activating signal (the costimulator)

A

it undergoes clonal anergy

39
Q

what is the benefit of T-cells becoming anergic if they don’t revceive a costimulator

A

this can be good if the T-cell wasn’t correctly screened against a self antigen in the periphery during development. so even if it binds the antigen, it wont work without a costimulator

40
Q

what is the third signal that helps in T-cell activation

A

cytokines

41
Q

what is the autocrine type of cytokine that helps in T-cell activation

A

IL-2 (autocrine means that it produces the cytokine and produces the receptor for it)

42
Q

does the binding of IL-2 to activating T-cells cause a strong response

A

yes, it causes a strong proliferation signal

43
Q

do Dendritic cells, macrophages, and B-cells have costimulatory characteristics

A

yes

44
Q

What are superantigens

A

a special class of T-cell activators. they are viral/bacterial proteins that bind to VB regions of TCRs and the alpha chain of class 2 MHC molecules

45
Q

what affect do superantigens have on T-cell activation

A

they essentially cause the T-cells to not need costimulation, and cause dramatic cytokine production by a lot of inappropriately activated T-cells
(cause T-cells to become overactive)

46
Q

what are the two types of Superantigens

A

exogenous (secreted by bacteria)

endogenous (viral gene produced cell membrane proteins)

47
Q

after a t-cell has received type 1 and 2 signals and become active it produces cytokines and their receptors, which causes activation and a robust proliferation of ___

A

memory and effector clonal cell populations

48
Q

What are the different types of helper T-cells

A 
TH1
TH2
Th17
TH REG
TFH
49
Q

What cytokine causes the proliferation of TH1 helper cells, and how does that happen?

A

IL-12

PAMPS are bound by PRRs on APCs. this causes them to secrete IL-12. and IL-12 causes proliferation of TH1 Helper cells

50
Q

What cytokine causes the proliferation of TH2 helper cells, and how does that happen?

A

IL-4

just like IL-12 (PRRs bind PAMPS and (On APCs and secrete IL-4) which causes the prouction of TH2 helper cells

51
Q

what microbe causes the production of TH1 helper cells via IL-12

A

viruses

52
Q

what microbe causes the production of TH2 helper cells via IL-4

A

worms

53
Q

what kind of Helper cells do worms cause to be proliferated

A

TH2 helper cells (Via IL-4)

54
Q

what kind of helper cells do viruses cause to be proliferated

A

TH1 helper cells (Via IL-12)

55
Q

What do TREG cells do

A

Regulate and suppress immune and inflammatory responses

56
Q

what do TH17 cells do

A

cause inflammation

57
Q

what doTH2 cells do

A

Allergic and anti-helminth responses

58
Q

what do TFH cells do

A

B cell help in germinal centers

59
Q

what do TH1 cells do

A

Cell mediated immunity, macrophage activation, inflammation

60
Q

Leprosy can affect the differentiation of T-cells. Which type of leprosy stimulates which type of T cell

A

Tuberculoid leprosy stimulates a TH1 response

Lepromatous leprosy stimulates a TH2 response

DMD 5244 (Immunity) (16 decks)

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