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Related Experiment Video

Updated: May 28, 2026

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

IL-6 Exacerbates Experimental Autoimmune Prostatitis by Disrupting STAT5a-Mediated Treg Cell Function and Th17/Treg

Xianhong Liu1,2,3, Xiaokang Bian1,2,3, Shanchuan Han1,2,3

  • 1Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, China, ahmu.edu.cn.

Mediators of Inflammation
|May 26, 2026
PubMed
Summary

Interleukin-6 (IL-6) drives immune imbalance in experimental autoimmune prostatitis (EAP) by disrupting T helper 17 (Th17)/regulatory T (Treg) cell balance and impairing Treg function. Targeting IL-6 may offer a therapeutic strategy for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS).

Keywords:
IL-6STAT5aTregchronic prostatitis/chronic pelvic pain syndrome

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Area of Science:

  • Immunology
  • Urology

Background:

  • Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a prevalent urological condition.
  • Immune dysregulation, specifically involving T helper 17 (Th17) and regulatory T (Treg) cells, is implicated in CP/CPPS pathogenesis.
  • The upstream factors contributing to this Th17/Treg imbalance are not fully understood.

Purpose of the Study:

  • To investigate the role of interleukin-6 (IL-6) in the pathogenesis of experimental autoimmune prostatitis (EAP).
  • To determine if IL-6 is associated with altered Th17/Treg cell homeostasis and impaired Treg function in EAP.
  • To explore the potential of IL-6 as a therapeutic target for CP/CPPS.

Main Methods:

  • An EAP mouse model was established using NOD mice immunized with prostate antigen.
  • Flow cytometry was used to analyze Th17 and Treg cell populations.
  • Enzyme-linked immunosorbent assay (ELISA) measured cytokine concentrations.
  • Western blotting and immunohistochemistry assessed signal transducer and activator of transcription 5a (STAT5a) expression.
  • In vivo IL-6 inhibition and in vitro experiments evaluated the impact of IL-6 on T cell differentiation and function.

Main Results:

  • EAP mice exhibited significantly higher serum IL-6 levels compared to controls.
  • A notable imbalance in Th17/Treg homeostasis was observed in EAP mice, characterized by increased Th17 cells and decreased Treg cells.
  • Treg cell suppressive activity was diminished in EAP mice.
  • In vitro studies demonstrated that IL-6 promotes Th17 differentiation while suppressing Treg generation and function, partly via inhibition of STAT5a signaling.
  • Pharmacological inhibition of IL-6 partially restored Treg function and reduced inflammation in EAP.

Conclusions:

  • IL-6 plays a critical role in the Th17/Treg imbalance and Treg dysfunction observed in EAP.
  • The mechanism involves IL-6-mediated inhibition of STAT5a signaling in Treg cells.
  • Targeting IL-6-related pathways presents a promising therapeutic avenue for managing CP/CPPS.