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Glycoursodeoxycholic acid regulates peritoneal monocytic myeloid-derived suppressor cells to alleviate systemic

Rui Wang1, Binghong Wang2, Bo Li2

  • 1Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Disease, Shanghai, China; Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.

Journal of Autoimmunity
|April 9, 2026
PubMed

Insights

Monocytic myeloid-derived suppressor cells (M-MDSCs) in decompensated cirrhosis ascites protect against immune dysfunction. Glycoursodeoxycholic acid (GUDCA) and TREM2 are key regulators, offering potential therapeutic targets for immune restoration.

Area of Science:

  • Immunology
  • Hepatology
  • Metabolomics

Background:

  • Decompensated cirrhosis involves cirrhosis-associated immune dysfunction (CAID).
  • Peritoneal immune landscape and monocytic myeloid-derived suppressor cells (M-MDSCs) roles are not fully understood.
  • Ascites metabolites may influence immune cell function.

Purpose of the Study:

  • Characterize the peritoneal immune landscape in decompensated cirrhosis.
  • Focus on M-MDSCs and their association with clinical outcomes.
  • Investigate regulatory mechanisms involving ascites metabolites.

Main Methods:

  • Prospective study of 55 decompensated cirrhosis patients (survivors vs. non-survivors).
  • Flow cytometry analysis of ascites and peripheral blood immune cells.
  • Targeted metabolomics of ascites and in vitro M-MDSC differentiation with glycoursodeoxycholic acid (GUDCA).

Main Results:

  • Survivors showed higher frequencies of immunosuppressive M-MDSCs in ascites.
  • Elevated ascites GUDCA levels correlated positively with M-MDSC levels in survivors.
  • In vitro, GUDCA enhanced M-MDSC suppressive capacity via the TGR5-TREM2-oxidative phosphorylation axis; TREM2 expression predicted improved survival.

Conclusions:

  • Peritoneal M-MDSCs play a protective role in decompensated cirrhosis immune dysfunction.
  • GUDCA and TREM2 are key regulators of M-MDSC function.
  • These findings suggest potential immunomodulatory strategies for restoring immune balance.
Abstract

Keywords:
Bile acidCirrhosis-associated immune dysfunctionMyeloid-derived suppressor cellTriggering receptor expressed on myeloid cells 2

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