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Immunology and Infection > CD4 T cells > Flashcards

CD4 T cells Flashcards

1
Q

what are the different subsets of CD4 T cells?

A
  • Th1
  • Th2
  • Th17
  • Treg
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2
Q

how are the different CD4 T cells distinguished?

A

by their signature cytokines

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3
Q

what is the signature cytokine of Th1?

A

IFN-y

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4
Q

what is the signature of Th2?

A

IL-4, IL-5

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5
Q

why are different subsets of CD4 T cells needed?

A

different pathogens need different immune responses

- the different subsets coordinate different distinct immune responses

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6
Q

what are cytokines?

A
  • proteins secreted by immune cells and non-immune cells that bind to receptors
  • secreted proteins that influence immune function
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7
Q

what is signal?

A

polarising cytokines

- innate immune cells evolved to produce different polarising cytokines following recognition of different pathogens

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8
Q

how does a CD4 T cell differentiate to a Th1?

A
  • DC recognises PAMP through PRR (eg bacteria)
  • DC presents peptide and produces IL-2
  • naive CD4 T cell has an IL-2R
  • type 1 innate lymphoid also has a IL-2R and produces IFN-y
  • Binds to IFN-yR on CD4 T cell
  • naive CD4 T cell becomes a TH1
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9
Q

what is Th1 cell characterised by?

A

high levels of IFN-y production

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10
Q

how does a CD4 T cell differentiate into a Th2?

A
  • parasitic worm secretes molecules
  • DC presents antigens on MHC II
  • parasitic worms cause tissue damage
  • tissue damage detected by stromal cells
  • produces cytokines that induce ILC2
  • ILC2 produces IL-4
  • naive CD4 T cell differentiates to a Th2 cell in response to the two signals
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11
Q

what is the general pathway of a polarising cytokine inducing intracellular signalling pathways in CD4 T cells?

A
  • cytokine binds receptor
  • conformational change
  • Activates JAKs
  • phosphorylates cytokine receptor
  • act as docking sites for STATs
  • bring STATs close to JAKs
  • JAKs phosphorylate STATs
  • STATs move into nucleus
  • act as transcription factors
  • interact with promoters
  • results in expression of cytokines, cytokine receptors and transcription factors
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12
Q

what s the lineage specific transcription factor of Th1?

A

T-bet

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13
Q

what is the lineage specific transcription factor of Th2?

A

GATA3

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14
Q

what happens as a result of IL-2 binding to the IL-2 receptor in Th1 cells?

A
  • conformational shift
  • activates JAKs
  • docking sites for STAT4, gets phosphorylated
  • STAT4 migrates to nucleus
  • binds to promoter of T-bet
  • causes expression of IL-2R
  • causes expression of IFN-y
  • T-bet binds and stabilises expression
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15
Q

what happens as a result of IL-4 binding to the IL-4 receptor on Th2 cells?

A
  • conformational shift
  • activates JAKs
  • phosphorylates STAT6
  • moves to the nucleus
  • interacts with the promoters of these 4 genes (and causes expression):
    1. GATA3 2. IL-4R 3. IL-4 4. IL-5
  • GATA3 binds and stabilises expression
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16
Q

what are Th1 good against?

A

bacteria, viruses, intracllular protozoa

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17
Q

what are Th2 good against?

A

parasitic worms

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18
Q

what is the general function of a CD4 T cell?

A
  • cause class switching in B cells
  • stronger activation of macrophages
  • stronger CD8+ activation
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19
Q

what is B cell class switiching?

A
  • antibodies have different isotypes
  • different variable and constant regions
  • start as IgM or IgD
  • class switch to become IgG, IgE, IgA
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20
Q

why is the antibodies different heavy chain constant regions important?

A
  • bind to different Fc receptors

- different ability to activate the complement cascade

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21
Q

how do CD4 T cells cause class switching in B cells generally?

A

through their signature cytokines

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22
Q

how does Th1 cause class switching?

A
  • produces IFN-y
  • binds to IFN-yR on B cells
  • induces B cells to class switch to IgG2a
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23
Q

how does Th2 cause class switching?

A
  • produces IL-4
  • binds IL-4R on B cells
  • induces class switch to IgG1 or IgGE
  • when class switched the antibodies bind to different immune cells
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24
Q

after being class switched by Th2 what affects do these antibodies have?

A
  • bind to different immune cells
  • eg in response to parasitic worms-IL-4-IL-4R- IgE produced, eosinophils and mast cells expresses a high affinity receptor (FceR) for IgE
  • also produces IL-5 which is a growth and survival factor for eosinophils
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25
what is FceR?
- binds to the Fc region of the antibody | - now described as being pre-armed with antibody
26
what happens when parasites produce factors that bind to the IgE receptors?
- can bind to the antibody on the surface - cross links the Fc receptors and causes the activation of eosinophils and mast cells and their degranulation - leads to damaging of the parasite
27
what do naive CD4 T cells express?
- express L selectin which allows it to circulate into the lymph nodes - express adhesion molecules like LFA1
28
what happens when naive CD4 T cells become activated?
- they have a different surface phenotype - lose expression of L-selectin (it is cleaved off) - increase in integrins - start expressing CD40L
29
why is CD40L needed?
involved in the interaction of macrophages and dendritic cells
30
where do CD4 T cells migrate?
from the blood to inflamed tissues
31
how do CD4 T cells migrate from the blood to inflammed tissues?
- macrophages release inflammatory cytokines and chemokines - increase expression of ICAM1 and VCAM1 - VCAM1 binds VLA-4 - activated T cell adheres and can migrate into the tissue - helps macrophages
32
why is it important to note that macrophages are also APCs?
- digest and present on MHC II to Th1 cells | - get cross talk
33
how do Th1 cells help macrophages?
- produce IFN-y which binds to IFN-yR on macrophages - produces CD40L which binds to CD40 - this elicits a membrane associated signal - activates macrophages to kill intracellular pathogens
34
how do DCs activate CD8 T cells?
- through the expression of peptide bound MHC I | - however, the activation is suboptimal
35
how does a CD4 T cell help to full activate a CD8 T cell?
- DC presents peptide MHC II - activates CD4 - produces large amounts of IL-2 - IL-2 nourishes CD8 - can also help through the CD40L - the active CD4 T cells licence the DC to fully activate the CD8 T cell
36
how does the CD4 T cell help the CD8 T cell with the CD40L?
- cross links with CD40 on DC - causes a signalling cascade from the DC - causes the DC to express new co-stimulatory molecules (4-IBBL) which binds to the co-receptor (4-IBB) - results in the strongest CD8 activation
37
what signature cytokine do Th17 cells produce?
IL-17
38
what is the role of a Th17 cell?
- to initiate effector immune response against pathogens that cannot be cleared by Th1 or Th2 cells - target extracellular bacteria and fungi
39
how are Th17 cells induced?
1. PAMPs bind to DC PRRs 2. DC produces signal 3 which activates TGF-B and IL-6 3. Initial Th17 differentiation 4. DCs also produce IL-23; IL-23 binds to IL-23R
40
what happens when PAMPs bind to DC PRRs during Th17 differentiation?
- antigen uptake - digested into peptides - MHC II presentationss - PRRs toll like receptors and C type lectins
41
what is the role of TGFB and IL-6 during Th17 differentiation?
- IL-6: inflammatory cytokine. Binds to receptors on endothelial cells and express more adhesion molecule - Active TGFB: converts inactive TGFB in the environment to active TGFB (cleaves it)
42
what effect does IL-23 have when it binds to IL-23R during Th17 cell differentiation?
- stabilised the phenotype | - promotes survival and expansion of Th17 cells
43
what happens during the STAT3 intracellular signalling pathway when IL-6 binds to the IL-6R on Th17?
- conformational shift - activates JAKs - phosphorylates the IL-6R - STAT3 docks and is phosphorylated - STAT3 migrates to the nucleus and interacts with the promoters: 1. binds RORyt 2. more expression of IL-23R 3. more expression of IL-17 - STAT3 alone generates a small amount of expression
44
what happens during the TGF B intracellular signalling pathway when IL-6 binds to the IL-6R on Th17?
- not as well understood - TGFB - TGFB receptors - activates SMAD proteins - they go to the nucleus and interact with the same genes as STAT3 - get full expression of Th17 genes: RORyt, IL-23R and IL-17 - RORyt binds back and stabilises expression
45
how does Th17 become activated?
- by DCs in the T cell zone causing Th17 differentiation | - tissue macrophage reactivate Th17 cells through MHC II
46
how do Th17 cells get into the site of infection?
- become activated by DCs - leave the lympho node - gain VLA4 and increase LFA1 - interacts with adhesion molecules and chemokines - enters the tissue
47
what is the function of the IL-17 chemokine that Th17 cells release?
- bind to IL-17R - expressed by fibroblasts and epithelial cells - these stromal cells produce lots of CXCL8 - attracts neutrophils
48
what is the role of Th17 cells?
inducing stromal cells to recruit neutrophils to the site of infection
49
what is the role of Tregs?
- turn of the immune response | - they are inflammatory and potentially pathogenic
50
what are the 2 types of Tregs?
natural Treg and induced Treg - have alpha beta TCR - have CD4 on surface - inhibit effector T cells - inhibits APC - inhibits other immune cells
51
what cause natural Tregs to differentiate in the thymus?
- nTregs develop in the thymus in response to stronger than normal signal through TcR stimulation - thymocyte upregulates FoxP3
52
what is meant by a stronger than normal reaction in nTregs?
- bind to self-peptide MHC II not strong enough that they are autoreactive but to an extent that it can become activated regulatory cytokines
53
what is hypothesised about nTregs?
that nTregs are all self-reactive - inhibit strongly auto-reactive T cells that could cause autoimmunity
54
what causes induced Tregs to differentiate in the periphery?
- start as naive T cells - encounters DC presenting its antigen and co-stimulation, able to activate TGFB in the absence of an inflammatory signal
55
what is the default state for T cell that encounters a DC presenting its antigen in the absence of an inflammatory signal?
this T cell will upregulate FoxP3 and differentiate into iTreg
56
what is the difference between the activation of an iTreg and Th17?
- iTreg needs TGFb (immune suppression) - Th17 needs TGFB and IL-6 (inflammation) - pathogens induce inflammatory cytokines that switch immune suppression to an inflammatory response
57
how do Tregs suppress the immune response?
through cell surface molecules and secretion of immune supressive cytokines
58
what cell surface molecules do Tregs use to suppress the immune response?
1. Tregs express high levels of CTLA-4 | 2. Tregs express high levels of IL-2 receptors
59
what is the role of CTLA-4 in Treg immune suppression?
- high affinity to CD80/CD86 on DCs - sequesters them away from naive T cells - stops DCs providing signal 2 to naive T cells (anergy) - CTLA-4 can physically rip CD80/CD86 from APCs
60
what is the role of IL-2R in Treg immune suppression?
can suck the IL-2 away from the activated T cells to stop their proliferation
61
what is the role of the immunosuppressive cytokines IL-10 and TGFB in Tregs?
1. inhibit IL-12 production by DCs 2. Reduce mHCII and CD80/CD86 levels on DCs 3. inhibit T cell proliferation 4. generate more Tregs (TGFB)
62
how have Foxp3(+) regulatory T cells been shown to be essential?
- natural mutations to Foxp3 on X chromosome = IPEX syndrom - they lack Tregs - fatal early onset and autoimmune disease in males

Immunology and Infection (13 decks)

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