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Updated: Aug 28, 2025

Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation
07:46

Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation

Published on: October 25, 2024

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γ-Tocotrienol inhibits T helper 17 cell differentiation via the IL-6/JAK/STAT3 signaling pathway

Hanqing Zhao1, Xin Guo1, Yunxuan Lei1

  • 1Department of Immunology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai Institute of Immunology, Shanghai 200025, China.

Molecular Immunology
|September 20, 2022
PubMed

Insights

Gamma-tocotrienol (GT3) suppresses T helper 17 cell differentiation by inhibiting the IL-6/JAK/STAT3 pathway. This vitamin E compound also reduced disease severity in a mouse model of psoriasis.

Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • γ-Tocotrienol (GT3), a vitamin E derivative, possesses known medicinal properties.
  • The precise role of GT3 in T helper 17 (Th17) and regulatory T cell (Treg) differentiation and function remains unclear.
  • Th17 cells are implicated in various autoimmune diseases, making their regulation a key therapeutic target.

Purpose of the Study:

  • To investigate the effect of γ-tocotrienol (GT3) on T helper 17 (Th17) cell differentiation and function.
  • To elucidate the molecular mechanisms underlying GT3's influence on Th17 cells.
  • To evaluate the therapeutic potential of GT3 in an in vivo model of inflammation.

Main Methods:

  • In vitro assessment of Th17 differentiation with GT3 treatment.
  • Analysis of signal transducer and activator of transcription 3 (STAT3) phosphorylation in the interleukin 6 (IL-6)/Janus kinase (JAK)/STAT3 pathway.
  • Evaluation of hypoxia-inducible factor 1-alpha (HIF1A) expression in Th17 cells.
  • In vivo study using an imiquimod (IMQ)-induced psoriasis-like mouse model.

Main Results:

  • GT3 suppressed Th17 cell differentiation in vitro.
  • GT3 inhibited STAT3 phosphorylation within the IL-6/JAK/STAT3 signaling pathway.
  • GT3 reduced HIF1A expression, impacting Th17 cell metabolism.
  • In vivo, GT3 treatment ameliorated disease severity in the IMQ-induced psoriasis model by decreasing splenic Th17 cell populations.

Conclusions:

  • γ-Tocotrienol (GT3) effectively suppresses Th17 cell differentiation and function.
  • The mechanism involves the inhibition of the IL-6/JAK/STAT3 signaling pathway and modulation of Th17 cell metabolism.
  • GT3 demonstrates therapeutic potential for inflammatory conditions like psoriasis by targeting Th17 cells.
Keywords:
Cell differentiationJAK-STAT pathwayPsoriasisT helper 17 cellsγ-Tocotrienol

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