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CMOD- Block1 > Immuno 8: T Cell Effector Mechanisms > Flashcards

Immuno 8: T Cell Effector Mechanisms Flashcards

1
Q

A casual reminder:

What is an effector T cell?

A

A fully differentiated T cell that is ready to perform its immune function. Does not require co-stimulation by C7.

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2
Q

How do effector (armed) T cells differ from their unarmed (liberal, passivist) precursors?

A

1- Armed T cells do not require co-stimulation by C7 to perform functions.
2- They express an array of adhesion molecules that direct them to appropriate tissues.

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3
Q

List the cell-surface molecules found on resting, non-activated T cells.

A

L-selectin
LFA-1
CD2 - adhesion and co-stim. molecule on T cells and NK cells
CD4
TCR
CD44 - ECM component of conn. tissue and epi. tissue
CD45RA - only found on naive T cells

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4
Q

List the cell-surface molecules found on activated (Effector) T cells.

A

VLA-4
LFA-1 ++
CD2 ++ -adhesion and co-stim. molecule on T cells and NK cells
CD4
TCR
CD44 ++ - ECM component of conn. tissue and epi. tissue
CD45RO - only found on activated and memory T cells

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5
Q

Just for fun, list the 3 main types of effector T cells.

A

CD8+ effector T cells

CD4+ helper T cells (Th1 and Th2)

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6
Q

What is the primary function of CD8+ T cells?

A

Kill affected cells, resulting in premature termination of the replicative cycle of the pathogen.

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7
Q

What are the effector molecules that CD8 cells produce that are responsible for their host cell killing function?

A

Fas Ligand
perforin
granzymes
granulysin

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8
Q

What are the cytokines secreted by CD8 cells that are involved in development of immune responses?

A

Interferon-gamma (INF-gamma)

Lymphotoxin (LT)

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9
Q

What is the primary role of CD4 T cells?

A

Supply critical secondary activation stimuli that are needed to activate an antigen-specific B cell and to drive their differentiation.

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10
Q

Do both Th1 and Th2 cells function to supply critical secondary activation stimuli that are needed to activate an antigen-specific B cell and to drive their differentiation?

A

Yes.

Th1 cells also function to activate macrophages, making them (macrophages) more phagocytic and bacteriocidal.

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11
Q

In addition to the Th1 and Th2 helper T cells, there are two additional CD4+ effector T cell types. Name them.

A

Tregs

Th17 cells

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12
Q

What is the function of Tregs?

A

prevent activation of self-reactive T cells

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13
Q

What is the function of Th17 Cells?

A

induce production of neutrophil chemoattractants and antimicrobial peptides by several cell types.

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14
Q

In the co-stimulation step of activating a naive T cell, C7 on the APC binds to _______ on the naive T cell.

A

C7 on the APC binds to CD28 on the T cell

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15
Q

When co-stimulatory signals are received, the T cell begins to proliferate (driven by the autocrine growth factor, ______).

A

IL-2

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16
Q

Perforin is an effector molecule produced by CD8 cells to kill host cells infected with intracellular pathogens. How does it work?

A

Inserts into host cell membranes as a multimer complex (similar to MAC), forming pores in the cytoplasmic membrane of the cell.

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17
Q

Granulysin is an effector molecule produced by CD8 cells to kill host cells infected with intracellular pathogens. How does it work?

A

Forms pores in the cytoplasmic membrane of host cells. Appears to have antimicrobial properties.

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18
Q

Granzymes are effector molecules produced by CD8 cells to kill host cells infected with intracellular pathogens. How do they work?

A

Serine proteases that initiate the apoptotic pathway (via caspase cascade) if they gain access to the host cell cytoplasm.

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19
Q

How do granzymes get into the cytoplasm of an affected host cell to initiate apoptosis?

A

Since perforins only make pores that are 6-8kD wide and granzymes are 30-60kD wide, what we THINK happens, is that the action of perforins stimulates the host cell to endocytose that portion of the cell membrane for repair. Granzymes closely associate with the membrane pore formed by the perforins and are inadvertently brought in by the host cell.

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20
Q

What does IFN-gamma do, anyways?

A

Drives the differentiation of Th0 T cells toward a Th1 phenotype. This is important because Th1 responses are critical for clearance of most intracellular pathogens. That’s why CD8, in particular, releases IFN-gamma.

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21
Q

What does Fas ligand do, bro?

A

Fas ligand is a bro-tein that can initiate (like in a Frat, bro) programmed cell death by binding to Fas on the surface of host cells, bro.

22
Q

Fas ligand binds to how many copies of Fas, all at once?

A

3 copies.

23
Q

Once the Fas ligand:Fas bond forms, what happens next, ultimately resulting in cell death?

A

The intracellular domains of Fas undergo conformational changes that make them a template for binding by adaptor proteins that have so called “death domains”. These proteins recruit caspase 8, which in turn cleaves caspase 3. Caspase 3 then cleaves I-CAD, activating CAD which goes into the nucleus and cuts up the cell’s DNA. The cell is effectively dead, at this point.

24
Q

How many signals do Effector T cells require to begin their duties?

A
  1. Just need to bind to their cognate peptide. Then they go to WORK.
25
Q

How many infected host cells can CTL cells (CD8+) kill?

A

Many, over the course of their lifetime.

26
Q

Will CTLs kill cells not bearing their cognate antigen?

A

No, silly!

27
Q

What is required to bring a CTL and possibly infected cell together in close enough proximity for the CTL to sample the peptide:MHC complex?

A

LFA-1 on the CTL binds to ICAM on the host cell.

28
Q

How to CTLs not kill the neighboring, non-infected cells of those they are trying to kill when they release their cytotoxic granules?

A

They polarize the granules to the side facing the target cell and release from there.

29
Q

Who tells macrophages to get “highly-activated” and kill their intracellular pathogen guests?

A

Th1 cells, dude!

30
Q

How does a Th1 CD4 cell tell a macrophage it recognizes as infected (via MHC class II on macro’s surface), to kill its rowdy inhabitants?

A

1- CD-40 ligand on the T cell binds to CD40 on the macrophage
2- the T cell will produce IFN-gamma that binds to IFN-gamma receptors on the macrophage.

31
Q

A macrophage, once activated, is now better at two things. List them.

A 
1- killing the little shits it ate (Oxygen radicals/nitric oxide)
2- Upregulates expression of MHC class I and II as well as B7, making it a better APC. Because before this, it was a pretty shitty APC, let's be honest...
32
Q

What happens is a macrophage is worn out and too old, tired or demented to kill its intracellular pathogens?

A

Th1 cells bind to them via Fas and signal for their self destruction via apoptosis. (Fas-adaptor protein-Cas8-Cas3-ICAD-CAD-DEATHHAAAH)

33
Q

Th1 cells produce IL-3 and GM-CSF, these cytokines induce what to do what?

A

Induce macrophage differentiation in the bone marrow.

34
Q

Th1 cells produce TNF-alpha and lymphotoxin, these cytokines do what?

A

Activate vascular endothelium, resulting in easier movement of macrophages (monocytes?) from the circulation into inflammatory tissue.

35
Q

B cells require what two activation signals to become activated?

A

1- recognition of their cognate antigenic determinant through their B cell receptor.
2- activation stimuli from helper T cells that consist of CD40-ligand of the T cell binding to CD40 on the surface of the B cell, and cytokine signals produced by the helper T cell

36
Q

Th1 cells produce cytokines that signal a developing B cell to undergo class switching to antibody isotypes that are weakly or strongly opsonizing?

A

Stongly opsonizing (IgG1 & IgG3)

37
Q

Th2 cells produce cytokines that signal a developing B cell to undergo class switching to antibody isotypes that are weakly or strongly opsonizing?

A

Weakly opsonizing (IgG2, IgG4, IGA, & IgE)

38
Q

When does a granuloma form and what is its function?

A

Occurs when microbe/foreign body resists destruction by macrophages. Function is to prevent dissemination of microbe/foreign body

39
Q

What T cell type are required for granulomas to form?

A

Th1

40
Q

Tregs have a limited TCR repertoire with specificities that are mostly limited to ______ determinants.

A

Self determinants

41
Q

When a Treg recognizes its cognate determinant and also receives an additional signal (CTLA-4 on Treg binding to C7 on APC), it will begin to produce and secrete these two anti-inflammatory cytokines that act to deter activation of T cells also sampling peptides on that APC.

A

TGF-beta & IL-10

42
Q

What two cytokines do Th17 cells secrete and what do they do?

A

Th17s secrete IL-17 and IL-22 which stimulate epithelial cells to produce neutrophil chemoattractants and anti-microbial proteins, respectively.

43
Q

What cytokine, produced by Th1 cells and CTLs, provides activation stimuli for macrophages, encouraging nitric oxide production?

A

Lymphotoxin (LT) previously known as TNF-beta

44
Q

What cytokine, produced by Th2 cells supports growth and survival of Th2 cells and also promotes class switching to IgE?

A

IL-4

45
Q

What cytokine, produced by Th2 cells is the primary driving signal for class switching of B cells to IgA and also promotes growth/differentiation of eosinophils?

A

IL-5

46
Q

What cytokine is produced by Th2 cells and Tregs and has anti-inflammatory effects that result in an inhibition of cytokine release by macrophages (also downregs expression of MHC II and C7), and also inhibits T cell activation?

A

IL-10

47
Q

IL-3 is produced by what cells and does what?

A

Produced by both Th1 and Th2 cells and CTLs and serves as a growth factor for hematopoietic progenitor cells in the bone marrow (similar effects to GM-CSF)

48
Q

This cytokine is an anti-inflammatory cytokine produced by Tregs. Its most important function is to prevent activation of self-reactive T cells.

A

TGF-beta

49
Q

This cytokine is produced by Th17 cells and serves as a signal for induction of antimicrobial peptide production by endothelial cells.

A

IL-22

50
Q

This cytokine is produced primarily by Th17 cells and serves as a signal for induction of neutrophil chemokines by endothelial cells.

A

IL-17

51
Q

Describe the basics of the JAK-STAT phosphorylation pathway.

A

A cytokine binds to a cytokine receptor whose intracellular domain is one of two needed to begin the signalling. A second receptor trots over and binds to the first, this causes phosphorylation. A protein called STAT comes over to the dimer and binds, which causes the STAT to be phosphorylated. Once phosphorylated, the STATs dimerize and move to the nucleus where they act as transcription factors for whatever the cytokine wants done.

CMOD- Block1 (36 decks)

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