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CMOD- Block1 > Immuno 7: T Cell Activation/Differentiation > Flashcards

Immuno 7: T Cell Activation/Differentiation Flashcards

1
Q

Naive T cells can only be activated by what?

A

a professional antigen presenting cell (APC) bearing the T cell’s cognate peptide in an MHC molecule

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2
Q

What are naive T cells doing before they are activated?

A

they are circulating throughout the bloodstream, moving from secondary lymphoid tissue to secondary lymphoid tissue, just looking for dendritic cells to present its antigen to it

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3
Q

What is an HEV?

A

high endothelial venule; a naive T cell will have to cross the HEV wall to enter a secondary lymphoid tissue

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4
Q

T cells express ____s on their surface that bind to ____s onthe surface of HEV cells.

A

selectins; addressins

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5
Q

Interaction of what specific molecules initiates the “rolling” process that leads to diapedesis of T cells into lymphoid tissue?

A

L-selectin on T cells interacts with addressins GlyCAM-1 and CD34 on HEV cells

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6
Q

What is LFA-1 and what activates it?

A

LFA-1 = lymphocyte function-associated antigen; activated by chemokines on the HEV cell surface

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7
Q

What does LFA-1 bind to and what is the result?

A

LFA-1 binds ICAM-1; result is tighter interaction that allows the T cell to squeeze between two endothelial cells and enter the lymphoid tissue

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8
Q

What is the crucial factor for initiation of adaptive immune response?

A

the high daily rate of T cells sampling peptides presented on dendritic cells

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9
Q

What adhesion molecules on the surfaces of T cells bind to adhesion molecules on the surface of APCs?

A

LFA-1 –> ICAM-1 or -2
CD2 –> LFA-3
ICAM-3 –> LFA-1

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10
Q

If the T cell encounters its cognate peptide:MHC complex on an APC, LFA-1 on the surface of the T cell undergoes a conformational change that does what?

A

increases its affinity for ICAMs

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11
Q

What are the 3 types of professional APCs, and what pathogen is each specialized for?

A
  1. dendritic cells - viral and EC antigens
  2. macrophages - EC independently replicating microbes (e.g., bacteria and yeast) and IC antigens
  3. B cells - soluble antigens from IC and EC sources
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12
Q

What do APCs have on their surface that distinguishes them from all other cells in the body?

A

the co-stimulator molecule, B7

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13
Q

The binding of B7 to ___ on T cells is an interaction required for activation of a naïve T cell.

A

CD28

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14
Q

There are two signals that are required for T cell activation. What are they?

A

1) binding of the TCR to its cognate peptide in the context of MHC
2) co-stimulation signaling that results from interaction between B7 (on the APC) and CD28 (on the T cell)

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15
Q

Where do immature dendritic cells hang out?

A

under the surface epithelium and in solid organs

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16
Q

True or false: immature dendritic cells are very active in presenting antigen.

A

False - they are very active in taking up antigens

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17
Q

What signals dendritic cells to migrate to lymphoid tissue?

A

infection - recognizes a pathogen by its PRRs; takes up the antigen and migrates to a T cell center to mature and present the antigen

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18
Q

What’s the difference between immature and mature dendritic cells?

A

mature dendritic cells will express co-stimulatory molecules and high levels of MHC molecules on their surface, as well as adhesion molecules (ICAM-1 & -2, LFA-1 & -3); mature cells also produce a chemokine DC-CK for attracting naive T cells

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19
Q

What is DC-CK and what does it do?

A

it’s a chemokine (chemotactic cytokine) secreted by mature dendritic cells that attracts naive T cells

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20
Q

What are immature dendritic cells of the skin called?

A

Langerhans’ cells

**not to be confused with Langhans cells, which are multinucleated giant cells

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21
Q

Macrophages are scavenger cells. How do they end up presenting antigens to T cells?

A

they phagocytize and destroy many microbes, present the peptides on the surface. They can do this even in the absence of bacterial products (non-infectious agents)

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22
Q

How much MHC class II and B7 is expressed by resting macrophages?

A

not very much - very low levels of MHC class II and no B7

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23
Q

What happens to the levels of MHC class II and B7 on the surface of macrophages when they take up and process microorganisms?

A

MHC class II and B7 expression is upregulated for facilitated antigen presentation

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24
Q

How do macrophages participate in peripheral T cell tolerance?

A

when they encounter antigen in the absence of bacterial products they will take up and express peptides at low levels, but they will still not express B7. This results in T cell recognition of the MHC:peptide complex, but without co-stimulation so the T cell is anergized instead of activated

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25
Q

After binding an antigen, B cells will ____ and ____ the antigen, then present the peptide on MHC class __ molecules.

A

internalize and process; MHC class II

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26
Q

True or false: B cells constitutively express low levels of MHC class II molecules and high levels of B7 co-stimulator molecules.

A

False - they constitutively express HIGH low levels of MHC class II molecules and LOW levels of B7 co-stimulator

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27
Q

A T cell that recognizes its specific antigen bound to MHC, but does not receive the co-stimulation signal, will become ____.

A

anergic

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28
Q

Co-stimulation of the T cell in the absence of specific antigen will have what effect?

A

no effect…wah wah.

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29
Q

Activation of a CD8+ T cell by an APC other than a dendritic cell requires what?

A

that both the CD8+ and a CD4+ T cell must recognize antigen on the APC simultaneously. This is a mechanism of increased co-stimulation that is needed to activate the CD8+ T cell because it’s so destructive.

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30
Q

What makes dendritic cells special in activating T cells?

A

dendritic cells have intrinsically high so-stimulation activity which is significant enough to meet the threshold of CD8+ co-stimulation activity

31
Q

What is the role of IL-2 in T cell activation?

A
  1. it is produced by T cells upon activation
  2. T cells express a receptor with moderate affinity for IL-2, but activated T cells express a high-affinity form of the IL-2 receptor so they can bind better to lower concentrations of it
  3. T cells binding IL-2 via the high affinity receptor allows it to proliferate 2-3 times per day for several days
32
Q

What’s the difference between the lower and the higher affinity IL-2 receptors?

A

the lower affinity receptor has only a beta and a gamma chain, whereas the higher affinity receptor has a beta, gamma, and alpha chain

33
Q

What is an armed effector T cell?

A

It’s what Komron would be if he were an immune cell.

LOLOL- also a fully differentiated T cell that is ready to perform its effector function. Requires no co-stimulation.

34
Q

But for real, what is an armed effector T cell?

A

it’s a T cell that can produce all of the proteins that are required for its specialized function, they require no co-stimulation, they express higher levels of adhesion molecules LFA-1 and CD2, lose L-selectin because they no longer need to recirculate, and they express VLA-4 (adhesion molecule)

35
Q

Activated T cells differentiate into effector T cells after how long?

A

about 4-5 days of rapid proliferation the activated T cells will differentiate into effector cells, and are then able to respond to antigen without co-stimulation

36
Q

What are the 3 primary classes of effector T cells?

A
  1. Effector CD8 T cells, aka cytotoxic killer T cells
  2. Type I helper T cells, aka Th1 CD4 cells
  3. Type II helper T cells, aks Th2 CD4 cells
37
Q

What is the main function of cytotoxic killer T cells?

A

to recognize MHC I-bound peptides presented on the surface of infected [nucleated] cells and kill them

38
Q

What is the main function of Th1 CD4 cells? (Type I helper T cells)

A

involved in the cell-mediated immune response (intracellular infections); recognize peptides in the MHC II complex on macrophages or B cells

39
Q

Type I helper T cells produce ____ that stimulate ____ and ____ cells.

A

cytokines; macrophages and B cells

40
Q

Cytokines from what kind of effector T cells influences class switching and initiates somatic hypermutation in B cells?

A

Type I helper T cells

41
Q

What is the main function of Th2 CD4 cells? (Type II helper T cells)

A

involved in the development of the humoral immune response (extracellular infections)

42
Q

Th2 CD4 cells recognize antigens bound to MHC class ___ molecules presented on the surface of __ cells (primarily). They then supply _____ that influence class switching and induce somatic hypermutation.

A

MHC class II; B cells; cytokines

43
Q

True or false: CD8 cells emerging from the thymus will become cytotoxic killer T cells, and CD4 cells are undecided when they leave the thymus.

A

True dat.

44
Q

Th0 CD4 cells can become ___ or ___ cells.

A

Th1 or Th2 cells

45
Q

IL-2 and IFN-gamma tend to cause a Th0 cell to become a Th_ effector T cell.

A

1

remember: I from interleukin and I from interferon and 1

46
Q

IL-4 and IL-6 tend to cause a Th0 cell to become a Th_ effector T cell.

A

2

remember: 2-4-6

47
Q

Name two important factors in the decision of a Th0 cell to become either a Th1 or Th2 effector T cell.

A
  1. cytokine environment

2. nature and amount of antigen presented

48
Q

TH0 cells that are presented with low affinity or low concentration of antigen to the TCR tend to differentiate into TH__ cells, while TH0 cells that are presented with high affinity or high concentration of antigen to the TCR tend to differentiate into TH__ cells.

A

2; 1
*logic: intracellular infections will have lots of pathogen within the cell, that creates a high concentration and thus TH1 differentiation is favored in this environment

49
Q

What are the 3 characteristics of T regs?

A
  1. self antigen specific T cell receptors
  2. CD25 expressed on surface
  3. transcriptional repressor called FoxP3
50
Q

Th0 cells differentiate into Treg cells when they are in the presence of ____. This occurs during ____ development and is antigen-____.

A

TGF-beta; thymic development; independent

51
Q

What happens when Tregs recognize their cognate self antigen?

A

they produce anti-inflammatory mediators, cytokine IL-10 and TGF-beta

52
Q

Deficiency of FoxP3 results in what?

A

fatal autoimmune disease directed at a variety of host tissues; gut almost always affected, and other common targets are thyroid, pancreatic beta cells, and the skin

53
Q

Th17 cells are a recently discovered subset of T helper cells that produce what interleukins?

A

IL-17, IL-22, and IL-21

54
Q

A newly discovered subset of helper T cells that produce TGF-β, IL-10 are ____ cells.

A

TH3 cells

55
Q

Selectins bind to ____; and integrins bind to the ____ superfamily members.

A

addressins; immunoglobulin

56
Q

An addressin known as sulfated sialyl-Lewis X is also called ____ and binds ____.

A

GlyCAM-1; L-selectin

57
Q

One interaction that can occur between naive T cells and HEV endothelial cells is chemokine recognition. When T cell chemokine receptors bind chemokines on the endothelium, what happens within/to the naive T cell?

A

signaling is transduced to the nucleus of the naive T cell and integrins known as LFA-1 on the T cell surface are activated, leading to increased interaction with the endothelium

58
Q

Activated LFA-1 binds with relatively high affinity to what on the endothelial cells surface?

A

ICAM-1

59
Q

L-selectin on the naive T cell surface can bind what on the surface of HEV cells?

A

either GlyCam-1 (aka sulfated sialyl Lewis X) or CD34

60
Q

Activated T cells express the integrin ____ which can bind to ____ expressed on activated endothelial cells (activated because they are in an inflamed tissue).

A

VLA-4; VCAM-1

remember: v in activated) (<–that may or may not be a stretch…

61
Q

In the naive T cell - dendritic cell interaction, ___ on T cell surface binds ____ on the DC surface.

A

LFA-1 on the T cell binds ICAM on the DC

62
Q

If each individual adhesion molecule interaction has only a moderate affinity, how do T cells and APCs interact strongly enough to adequately sample the antigen?

A

Avidity: there are many copies of the adhesion molecules interacting for the antigen, and their combined strength is enough to cross the threshold; then the antigen binding causes a conformational change in LFA-1 that increases affinity for its ICAM

63
Q

After thymic development, what is the “back-up” mechanism that recognizes and removes most self-reactive T cells from the repertoire?

A

the need for B7 co-stimulation; if a T cell recognizes it cognate peptide in the circulation, it will bind, but if there’s no co-stimulation along with it then the T cell will become anergic and die

64
Q

What happens when a macrophage takes up both pathogen and self protein?

A

The proteins will be presented on MHC molecules, and the presence of the pathogenic protein pieces (recognized by PRRs) will upregulate B7. This will enable any self-reactive T cells to bind the self-protein, get co-stimulated because B7 is now present, and become activated against self proteins. Hence the belief that most autoimmune diseases are initiated during infections with a pathogen. This is also similar to the function of a vaccine.

65
Q

What are the transcription factors that drive expression of cytokines in effector T cells Th1, Th2, and Tregs?

A
  • T-bet in Th1 cells
  • GATA-3 in Th2 cells
  • FoxP3 in Tregs
66
Q

What are the major cytokines expressed by effector T cells Th1, Th2, and Tregs?

A
  • IL-2 and IFN-gamma in Th1 cells
  • IL-4 and IL-5 in Th2 cells
  • TGF-beta and IL-10 in Tregs
67
Q

What facilitates neutrophil movement in between vascular endothelial cells and into inflammatory sites? (*double check this question with the podcast)

A

PECAM-1 and …?

68
Q

What adhesion molecule expressed on naive T cells is the most important facilitator of interactions with antigen-presenting cells? Which is the important molecule on activated (effector) T cells?

A

LFA-1; VLA-4

69
Q

What is CD34?

A

addressin located on the surface of HEV cells that binds to L-selectin on the surface of the naive T cell

70
Q

True or false: there is no cross-over in function between Th1 and Th2 cells. (*double check this question with the podcast)

A

False - keep inm in that they both perform each other’s functions, specifically providing secondary signals to B cells, but it’s a matter of majority and bias

71
Q

Which T cell type has a role in recruitment of neutrophils to infected tissue? (*double check this question with the podcast)

A

Th17 T cells are chemotractive for neutrophils

72
Q

Where do Tregs reside, and how do they perform their effector functions? (*double check this question with the podcast)

A

secondary lymphoid tissues; they produce TGF-beta, cytokines, and other things

73
Q

How do Hassall’s corpuscles lead to the production of Tregs? (*double check this question with the podcast)

A

they express thymic stromal lymphoprotein (TSLP) which acts on medullary dendritic cells, inducing upregulation of B7 and likely production of cytokines,

74
Q

Once the two required signals for T cell activation have been received, what is/are the most important product(s) that begin to be produced by that activated T cell?

A

IL-2. Initiates T cell proliferation.

CMOD- Block1 (36 decks)

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