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A negative feedback loop mediated by STAT3 limits human Th17 responses.

Harriet A Purvis1, Amy E Anderson1, David A Young1

  • 1Institute of Cellular Medicine, Musculoskeletal Research Group, Newcastle University, Newcastle upon Tyne NE2 4HH, United Kingdom.

Journal of Immunology (Baltimore, Md. : 1950)
|June 29, 2014
PubMed
Summary
This summary is machine-generated.

Signal transducer and activator of transcription 3 (STAT3) limits T helper 17 (Th17) cell formation in memory populations. This STAT3-driven negative-feedback loop, involving ATP, may prevent excessive inflammation and tissue damage.

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Area of Science:

  • Immunology
  • Cellular Biology
  • Molecular Biology

Background:

  • T helper 17 (Th17) cells are crucial in chronic inflammatory diseases.
  • STAT3 is essential for Th17 cell differentiation.
  • The role of STAT3 in regulating memory Th17 cell populations is not fully understood.

Purpose of the Study:

  • To investigate the role of STAT3 in a negative-feedback loop that limits IL-17-producing T cells in memory populations.
  • To elucidate the mechanism by which STAT3 regulates memory Th17 cell formation.

Main Methods:

  • Human memory CD4(+)CD45RO(+) T cells were activated at high (HiD) and low (LoD) densities.
  • STAT3 phosphorylation and expression of CD39 were assessed.
  • STAT3 and CD39 activity were transiently inhibited.
  • ATP receptor P2X7 was blocked.

Main Results:

  • Th17 cell numbers were significantly higher under LoD conditions compared to HiD.
  • STAT3 activation was stronger and more rapid in HiD cells.
  • Inhibiting STAT3 or CD39 enhanced Th17 cell numbers in HiD cultures.
  • Blocking P2X7 reduced Th17 responses in LoD cultures.
  • STAT3 negatively regulates Th17 cells by limiting ATP availability.

Conclusions:

  • STAT3 induces a negative-feedback loop limiting memory Th17 cell formation by controlling ATP levels.
  • This mechanism may serve to prevent tissue damage during chronic inflammation.
  • Targeting STAT3 signaling could enhance, rather than suppress, memory Th17 responses, offering therapeutic potential.