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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Regulation of Metabolism01:19

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Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...
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Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
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Related Experiment Video

Updated: Mar 13, 2026

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
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A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

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Interferon Regulatory Factor 4 controls TH1 cell effector function and metabolism.

Justus Mahnke1, Valéa Schumacher1, Stefanie Ahrens1

  • 1Institute of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Scientific Reports
|October 21, 2016
PubMed
Summary
This summary is machine-generated.

Interferon Regulatory Factor 4 (IRF4) is crucial for TH1 cell responses and metabolism. IRF4 deficiency impairs TH1 differentiation and proliferation by affecting cellular energy production.

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Area of Science:

  • Immunology
  • Cellular Metabolism
  • Molecular Biology

Background:

  • Interferon Regulatory Factor 4 (IRF4) is known to be essential for TH2 and TH17 cell development and CD8+ T cell differentiation.
  • The role of IRF4 in TH1 responses and its impact on cellular metabolism remained largely uncharacterized.

Purpose of the Study:

  • To investigate the function of IRF4 in TH1 cell responses during Listeria monocytogenes infection.
  • To elucidate the role of IRF4 in regulating the metabolic adaptation of TH1 cells.

Main Methods:

  • Utilized IRF4 knockout (IRF4-/-) mice and Listeria monocytogenes infection model.
  • Analyzed TH1 cell differentiation markers (T-bet, IFN-γ), proliferation, glucose uptake (2-NBDG), oxidative phosphorylation, and aerobic glycolysis in CD4+ T cells.

Main Results:

  • IRF4-/- mice exhibited significantly reduced numbers of listeria-specific TH1 cells.
  • IRF4-/- CD4+ T cells failed to differentiate into TH1 cells, showing decreased T-bet and IFN-γ expression, and limited proliferation.
  • Activated IRF4-/- CD4+ T cells displayed impaired glucose metabolism, including reduced glucose uptake, oxidative phosphorylation, and aerobic glycolysis.

Conclusions:

  • IRF4 is identified as a central regulator of TH1 responses and cellular metabolism.
  • Metabolic adaptation regulated by IRF4 is critical for TH1 cell proliferation and differentiation.
  • IRF4's function in regulating TH cell metabolism is proposed to be fundamental for all TH cell responses.