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PTEN ameliorates autoimmune arthritis through down-regulating STAT3 activation with reciprocal balance of Th17 and

Seung Hoon Lee1, Jin-Sil Park1, Jae-Kyung Byun1

  • 1The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.

Scientific Reports
|October 7, 2016
PubMed

Insights

PTEN protein, regulated by p53, ameliorates autoimmune arthritis by inhibiting STAT3 activation and Th17 cell differentiation. Loss of p53 exacerbates arthritis, highlighting PTEN

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Signal transducer and activator of transcription 3 (STAT3) inactivation is a therapeutic strategy for autoimmune arthritis.
  • PTEN (phosphatase and tensin homolog) is a tyrosine phosphatase that inhibits STAT3 activation.
  • PTEN expression, regulated by p53, influences the balance between Th17 and Treg cells in autoimmune arthritis.

Purpose of the Study:

  • To investigate the role of p53-regulated PTEN in experimental autoimmune arthritis.
  • To determine if PTEN ameliorates arthritis by inhibiting STAT3 activation and modulating T cell differentiation.

Main Methods:

  • Overexpression of PTEN in a mouse model of collagen-induced arthritis (CIA).
  • Assessment of CIA severity, T cell activation, and Th17/Treg cell populations.
  • Evaluation of STAT3 activation in the context of p53 deficiency.

Main Results:

  • Systemic PTEN overexpression reduced CIA severity and STAT3 activity.
  • PTEN overexpression decreased T cell activation and modulated Th17/Treg cell balance.
  • p53 deficiency led to decreased PTEN expression, increased STAT3 activation, exacerbated arthritis, and dysregulated Th17/Treg populations.

Conclusions:

  • PTEN plays a protective role in autoimmune arthritis by inhibiting STAT3 activation and Th17 differentiation.
  • p53-mediated regulation of PTEN is crucial for controlling autoimmune arthritis.
  • Targeting the STAT3-modulatory activity of PTEN presents a potential therapeutic approach for rheumatoid arthritis.

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