Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IMIN 371 > T cell differentiation, function and regulation > Flashcards

T cell differentiation, function and regulation Flashcards

1
Q

What are the polarizing cytokines, master transcriptional regulator, effector cytokines, effector function and role in disease of Th2 cells?

A
  • polarizing cytokines = IL-4
  • master ts regulator = GATA3
  • effector cytokines = IL-4, IL-5, IL-13 –> activate B cells
  • effector functions = combats helminths infection and activated esosinophils
  • role in disease = allergy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the polarizing cytokines, master transcriptional regulator, effector cytokines, effector function and role in disease of Th1 cells?

A
  • polarizing cytokines = IL-12, IFN-g, IL-18
  • master ts regulator = T-Bet
  • effector cytokines = IFN-g, TNF –> proinflammatory
  • effector functions = combats intracellular pathogens and activates macrophages
  • role in disease = tissue inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the three processes that Th1 cell use to activate DCs

A
  1. licensing of DCs to present to CD8+ T cells by CD40 activation
  2. chemokines that recruit more inflammatory cells
  3. cytokines that activate more inflmmatory cells via IFNg binding to IFNgR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why do Th1 cells activate macrophages? How do Th1 cells activate macrophages?

A
  • Th1 are very important for clearing bactering that replicate inside macrophages (e.g. TB)
  • signaling through CD40 and IFNgR promotes fusion of endosomes with lysosomes to promote killing of bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe how Th2 cells alternatively activate macrophages

A

IL-13 conditions macrophages to increase:
- Ag presentation
- co-stimulation, scavenger Rs (mannose R and dectin R) to fungal Ag.s
- chitinases to degrade fungal and insect chitin
- anti-flammatory cytokines such as IL-10 and factors (TGF-b) to promote would healing

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

Describe the cross-regulation of Th1 and Th2 cells

A
  • expression of one master ts regulator block expression of the other (T-Bet and GATA3 inhibit each other)
  • e.g. if there’s lots of IL-4 and some IL-12 –> Th2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe some general characteristics of Treg cells

A
  • develop in the periphery
  • secretes antiinflammatory cytokines
  • tumor treatments = shutting down Treg cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe how Treg cells create tolerance responses?

A
  1. express high levels of inhibitory CTLA-4 molecules that binds to CD80/86:
    - inhibit CD80/86 expression
    - increase IDO
    - decrease IL-6/TNFa (proinflammatory) production
  2. absorb IL-2 using IL-2R
  3. secrete antiinflammatory cytokines (IL-10 TGF-b) into the surrounding area, shutting down nearby cell’s reponses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Tregs secrete IDO, what does it do?

A

breaks down tyr, tyr is critical for T cell activation

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

What is the bystander suppression effect?

A
  • a Treg that interacts with an APC can supress T cells that engage seperate MHC-II complexes on the APC surface
  • “linked supression”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is an important site of functions for Tregs?

A

mucosal system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Job syndrome, where is the defect located, what are some characterisitcs?

A
  • Job syndrome = hyper IgE syndrome
  • defect = mutation in STAT3
  • recurrent skin and lung infections
  • elevated IgE levels in serum
  • unable to respond to IL-6 (trigger the function of Th17)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the cross-regulation of Th17 and pTreg cells

A
  • TGF-beta is a key cytokine for the differntiation of both subsets
  • IL-6 is the switch, allowing RORgT to dominate and induce Th17 subset and not Treg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why is a balance between Treg and Th17 cells ideal?

A
  • normal state could favor development of suppressive Treg population to keep inflammation controlled
  • inflammation from an infection (leading to IL-6 production) would stimulate more antibacterial Th17 differentiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is leprosy? Describe and name the two forms of leprosy observed

A
  • leprosy = bacteria replication inside macrophage vacuoles

tuberculoid:
- granulomas form and damage is limited to skin and nerves
- patient usually survives

lepromatous:
- extensive replication of bacteria
- fatal if untreated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

In leprosy, why does the same bacteria create different outcomes?

A
  • Th1 responses are required to control m. leprae
  • patients who developed lepromatous had a Th2 response instead of Th1
17
Q

What are CTL functions?

A
  1. make IFNg and TNFa
    - antiviral
    - induce MHC-I expression
    - activate macrophages
  2. induce death
    - cytotoxins (perforins and granzymes)
    - TNFa
    - FASL-FAS interactions
18
Q

Describe how CTLs induce cell death via degranulation, what proteins are important for production of an immune synapse?

A
  1. CTL TCR+CD8 binds to target cell MHC-I+Ag
  2. conjugate formation
  3. CTL cytoplasmic rearrangement
  4. CTL granules exocytose
  5. dissociatoin
  6. CTL recycling
  • LFA-1-ICAM-1 interactions are vey important for degranulation
19
Q

How does the conformation of LFA-1 change when a CTL is activated?

A
  • inactive = low affinity LFA-1 (lying down)
  • active = high affinity LFA-1 (standing)
20
Q

How are CTLs protected from perforin?

A
  • cathepsin B is a memb-bound protease that is located in the granules that contain perforin and granzymes
  • during degranulation, cathepsin B gets to the cell surface and degrades perforin that stays near the CTL membrane
21
Q

How do CTLS induce cell death through memb-bound TNFa?

A

mTNFa binds to TNFR1 on target cells and causes programmed cell death

22
Q

How do CTLS induce cell death through FAS activation?

A
  • FasL on CTL interacts with FAS on the target cell
  • activates downsream signals through a series of caspases
  • induces apoptosis
23
Q

Describe what occurs to end the T cell response

A
  1. Tregs decrease T cell activity
  2. co-inhibitory R’s (CTLA4, PD-1) are upregulated
  3. activation-induced cell death (AICD)
24
Q

Describe some characterisitcs of CTLA-4

A
  • expressed 24 hours after naive cells are activated
  • expressed at lower levels than CD28
  • binds to CD80/86 with greater affinity than CD28
25
Q

Describe the effects of PD-1 signaling

A
  1. limits proliferation
  2. limits cytokine production
  3. limits cytotoxicity
26
Q

Describe how AICD is triggered

A
  1. when naive T cells are activated they upregulate FAS, FASL and have high BCl-Xl levels
  2. if there is lack of Ag stimulation and cytokines, Bcl-Xl decreases and FASL trimerizes
  3. T cells trigger apoptosis in each other
27
Q

What is Canale-Smith syndrome: how is it caused, what does it cause?

A
  • caused by defective FAS-FASL
  • causes lymphoproliferative diseases
28
Q

What are FAS-FASL interactions important for in terms of reducing T cell activity?

A
  1. peripheral deletion of autoreactive T cells
  2. limiting T cell expansion
  3. shutting down T cell response

IMIN 371 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions