Podcast
Questions and Answers
How does CTLA-4 on Tregs suppress effector T cell activation?
How does CTLA-4 on Tregs suppress effector T cell activation?
- By secreting IL-2 to promote T cell proliferation, thus outcompeting effector T cells.
- By releasing granzymes and perforins to induce apoptosis in activated effector T cells.
- By competitively binding to B7 molecules on APCs, thus blocking co-stimulation of effector T cells and inducing endocytosis of B7 molecules. (correct)
- By directly stimulating effector T cells via co-stimulatory signals, leading to anergy.
If a patient with an autoimmune disease has a deficiency in FoxP3, what immunological effect would you expect?
If a patient with an autoimmune disease has a deficiency in FoxP3, what immunological effect would you expect?
- Reduced suppression by T regulatory cells, leading to increased autoimmune activity. (correct)
- Enhanced suppression of self-reactive B cells.
- Increased production of IL-2 by effector T cells.
- Decreased activity of cytotoxic T lymphocytes.
Why might IL-2 administration be a complex therapeutic strategy for autoimmune diseases?
Why might IL-2 administration be a complex therapeutic strategy for autoimmune diseases?
- IL-2 promotes the survival and proliferation of both effector T cells and Tregs, potentially counteracting the suppressive effects of Tregs. (correct)
- IL-2 directly activates macrophages, leading to increased inflammation.
- IL-2 induces the expression of FoxP3 in all T cells, leading to a general immune paralysis.
- IL-2 selectively inhibits the function of Tregs, exacerbating autoimmunity.
What mechanism do Tregs use to suppress the activation of self-reactive T cells by limiting their survival requirements?
What mechanism do Tregs use to suppress the activation of self-reactive T cells by limiting their survival requirements?
Which of the following is a primary mechanism by which Tregs suppress macrophage activity?
Which of the following is a primary mechanism by which Tregs suppress macrophage activity?
In a non-obese diabetic (NOD) mouse model, how do Tregs influence the onset of diabetes?
In a non-obese diabetic (NOD) mouse model, how do Tregs influence the onset of diabetes?
A researcher is investigating potential targets for enhancing Treg function in autoimmune disease therapy. Which molecule, when targeted for increased expression or activity, would likely enhance Treg-mediated suppression?
A researcher is investigating potential targets for enhancing Treg function in autoimmune disease therapy. Which molecule, when targeted for increased expression or activity, would likely enhance Treg-mediated suppression?
A study finds that a novel therapeutic agent increases TGF-β secretion specifically by Tregs. What downstream effects would be expected in the local microenvironment?
A study finds that a novel therapeutic agent increases TGF-β secretion specifically by Tregs. What downstream effects would be expected in the local microenvironment?
What role does cell-cell contact play in Treg-mediated suppression?
What role does cell-cell contact play in Treg-mediated suppression?
If a researcher aims to evaluate the efficacy of a new drug designed to enhance Treg function, which assay would best assess the drug's impact on Treg-mediated suppression?
If a researcher aims to evaluate the efficacy of a new drug designed to enhance Treg function, which assay would best assess the drug's impact on Treg-mediated suppression?
Flashcards
T Regulatory Cells (Tregs)
T Regulatory Cells (Tregs)
A subset of CD4+ T cells that suppress immune responses, expressing high levels of CD25 and CTLA-4, and regulated by Foxp3.
FoxP3
FoxP3
A transcription factor that regulates the development and function of T regulatory cells.
CTLA-4
CTLA-4
Molecule that competes with CD28 for binding to B7 on APCs, delivering an inhibitory signal to T cells.
CTLA-4 Function in T-regs
CTLA-4 Function in T-regs
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CD80/86
CD80/86
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T-regs and Self-reactive Lymphocytes
T-regs and Self-reactive Lymphocytes
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TGF-beta
TGF-beta
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IL-2
IL-2
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CD25
CD25
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IL-10 and Macrophages
IL-10 and Macrophages
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Study Notes
- T regs, a subset of CD4+ T cells, actively suppress the immune system by inhibiting lymphocyte activation and proliferation.
- Foxp3 regulates Tregs.
- Tregs limit the activation of self-reactive lymphocytes in the periphery by suppressing growth and limiting survival requirements.
- Tregs secrete TGF-beta to suppress the activation potential of self-reactive T cells.
- Survival of T regs depends on IL-2, depleting it from the microenvironment and limiting self-reactive T cells' access to this vital growth factor.
- Tregs express high levels of CTLA-4, outcompeting non-Tregs in binding with B7.
- IL-2 depletion, activated via the surface receptor and signaling through the Foxp3 transcription factor, limits the growth of self-reactive T cells.
- T regs are associated with suppressing autoimmune diseases like chronic colitis and autoimmune gastritis, making them potential targets for immune therapies.
Anti-inflammatory Function of Regulatory T Cells
- T regulatory cells prevent macrophages from secreting proinflammatory cytokines such as IL-1 and IL-6.
- T regulatory cells interact with macrophages, preventing them from activating other CD4+ T cells.
- T regulatory cells directly compete with CD4+ T cells for interleukin-2 (IL-2), which is important for the development of both CD4+ T cells and T reg cells.
- T regulatory cells secrete TGF-beta and IL-10, immune-suppressing cytokines that act on CD4+ T cells and other inflammatory mediators to reduce inflammation.
- A T regulatory cell can cause the destruction of T helper cells by using the perforin-granzyme pathway.
- T regulatory cells secrete IL-10, which acts directly on macrophages or other antigen-presenting cells.
- T regulatory cells have an inhibitory receptor known as CTLA-4, which interacts with CD80/86 (B7) on the surface of the macrophage, preventing the expression of several proinflammatory cytokines.
- T regulatory cells can prevent the early onset of several autoimmune diseases by providing anti-inflammatory responses.
- CTLA-4 plays a critical role in supressing immune responses.
- CTLA-4 helps regulate and surpress excessive immune activation in T regulatory cells.
- CTLA-4 competes with CD28 on CD4+ T cells for B7(CD80/86) binding on antigen presenting cells.
- CTLA-4 binding transmits an inhibitory signal while CD28 binding to B7 provides a stimulatory signal to T cells.
- Treg cells express high levels of CTLA-4, which allows them to effectively block co-stimulation of effector T cells.
- CTLA-4 acts as an immune checkpoint receptor.
- The Foxp3 nuclear transcription factor is expressed in T regulatory cells
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