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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
12:59

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

The nuclear orphan receptor NR2F6 suppresses lymphocyte activation and T helper 17-dependent autoimmunity

Natascha Hermann-Kleiter1, Thomas Gruber, Christina Lutz-Nicoladoni

  • 1Department for Medical Genetics, Molecular and Clinical Pharmacology, Medical University Innsbruck, 6020 Innsbruck, Austria.

Immunity
|August 15, 2008
PubMed

Insights

Nuclear receptor NR2F6 acts as a crucial regulator in T lymphocyte activation. This study reveals NR2F6

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Protein kinase C (PKC) is vital for T lymphocyte activation.
  • NR2F6 is a nuclear receptor with a known role in gene regulation.

Purpose of the Study:

  • To investigate the role of NR2F6 in CD4(+) T cell activation.
  • To elucidate the mechanism by which NR2F6 regulates T cell responses.

Main Methods:

  • Identifying NR2F6 as a PKC substrate.
  • Assessing NR2F6's effect on cytokine gene expression (IL-2, IL-17).
  • Analyzing NR2F6's interference with transcription factor binding (NF-AT, AP-1, NF-kappa B).
  • Utilizing Nr2f6-deficient mice to study in vivo immune responses.

Main Results:

  • NR2F6 antagonizes IL-2 and IL-17 expression in Th0 and Th17 CD4(+) T cells.
  • NR2F6 inhibits DNA binding of NF-AT:AP-1, repressing IL-17A promoter activity.
  • Nr2f6-deficient mice exhibit hyperreactive lymphocytes and increased susceptibility to autoimmune diseases.

Conclusions:

  • NR2F6 is a transcriptional repressor of IL-17 in Th17 cells.
  • NR2F6 plays a critical role in regulating T cell activation and preventing immunopathology.

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