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The Effects of CD100 Stimulation on Primary Human Hepatocytes (PHHs) and Its Implications in HBV-Related Liver

Chao Fan1, Xiaojun He2, Yun Zhou1

  • 1Department of Infectious Disease, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.

Journal of Gastroenterology and Hepatology
|October 21, 2025
PubMed

Insights

CD100 stimulation in liver cells shows potential for treating HBV-related liver cirrhosis by reducing fibrosis and activating anti-cirrhosis genes. This study investigated CD100

Area of Science:

  • Hepatology
  • Immunology
  • Molecular Biology

Background:

  • CD100 positively regulates immune responses and is implicated in Hepatitis B Virus (HBV) infection.
  • Its role in HBV-related liver cirrhosis, particularly its impact on hepatocytes, remains unclear.
  • Investigating CD100's function may reveal new therapeutic targets for liver cirrhosis.

Purpose of the Study:

  • To determine the impact of CD100 on hepatocytes and its role in HBV-related liver cirrhosis.
  • To explore CD100's potential as a therapeutic target for liver cirrhosis.
  • To elucidate the molecular mechanisms underlying CD100's effects in the liver.

Main Methods:

  • Analyzed serum sCD100 and platelet CD100 in HBV-infected patients.
  • Examined CD100 stimulation effects on primary human hepatocytes (PHHs) and gene expression via mRNA-microarray.
  • Assessed CD100's influence on hepatic stellate cell (HSC) activation and extracellular matrix (ECM) deposition in a co-culture system.

Main Results:

  • Serum sCD100 and platelet CD100 were downregulated in HBV-infected patients.
  • CD100 stimulation inhibited ECM deposition and promoted anti-fibrotic gene expression in PHHs and HSCs.
  • CD100 modulated PHH gene expression via plexin B1/B2, activating ERK and STAT3 signaling pathways.

Conclusions:

  • CD100 stimulation induces anti-cirrhosis gene expression in hepatocytes.
  • CD100 suppresses hepatic stellate cell activation via ERK and STAT3 signaling.
  • CD100 represents a potential therapeutic target for HBV-related liver cirrhosis.
Abstract

Keywords:
CD100HNF4ATGF‐β antagonistschronic hepatitis Bliver cirrhosisprimary human hepatocytes

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