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Isolation of Primary Human Decidual Cells from the Fetal Membranes of Term Placentae
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Isolation of Primary Human Decidual Cells from the Fetal Membranes of Term Placentae

Published on: April 30, 2018

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Phosphorylated STAT3 inhibited the proliferation and suppression of decidual Treg cells in unexplained recurrent

Bo Liu1, Huimei Wu1, Qianyi Huang1

  • 1Department of Reproductive Center, First Affiliated Hospital of Guangxi Medical University, Guangxi, China.

International Immunopharmacology
|March 11, 2020
PubMed

Insights

Hyperphosphorylation of signal transducer and activators of transcription 3 (STAT3) in decidual regulatory T (Treg) cells impairs their function in unexplained recurrent spontaneous abortion (URSA) patients. Inhibiting STAT3 phosphorylation restores Treg cell function, offering potential URSA treatment strategies.

Area of Science:

  • Immunology
  • Reproductive Biology
  • Cellular Signaling

Background:

  • Unexplained recurrent spontaneous abortion (URSA) is a complex reproductive disorder.
  • Decidual regulatory T (Treg) cells play a crucial role in maintaining pregnancy.
  • Dysfunctional Treg cells are implicated in the pathogenesis of URSA.

Purpose of the Study:

  • To investigate the effect of signal transducer and activators of transcription 3 (STAT3) phosphorylation on decidual Treg cell function in URSA patients.
  • To explore the underlying mechanism of STAT3 in URSA pathogenesis.
  • To identify potential therapeutic targets for URSA.

Main Methods:

  • Isolation of decidual Treg cells from URSA patients using magnetic beads.
  • Inhibition of STAT3 phosphorylation using Stattic.
  • Assessment of Treg cell proliferation and suppression via flow cytometry, real-time quantitative fluorescent PCR, and ELISA.
  • Detection of factors inducing Treg cell hyperphosphorylation.

Main Results:

  • URSA patients exhibited significantly increased STAT3 phosphorylation (pSTAT3) in decidual Treg cells.
  • pSTAT3 inhibited Treg cell proliferation by downregulating STAT5 and Foxp3 expression.
  • pSTAT3 reduced the secretion of immunosuppressive cytokines TGF-β1 and IL-10.
  • Pro-inflammatory cytokines IL-6 and IL-23 stimulated STAT3 phosphorylation in Treg cells.

Conclusions:

  • Hyperphosphorylation of STAT3 impairs crucial Treg cell functions, including proliferation, suppression, and cytokine secretion, contributing to URSA.
  • Inhibiting STAT3 phosphorylation can restore Treg cell function, suggesting a therapeutic avenue for URSA.
  • STAT3 signaling is a key factor in the pathogenesis of URSA.
Keywords:
Cell proliferationMaternal-fetal interfaceSTAT3Treg cellsURSA

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