The Dual Role of IP-10/CXCL10 in Liver Injury: From Pathogenic Mediator to Clinical Biomarker and Therapeutic Target

A complex interplay of immune and inflammatory mechanisms underlies liver injury, with the chemokine interferon-gamma-induced protein 10 (IP-10/CXCL10) playing a decisive role. Recent findings identify IP-10 as a key pathogenic mediator; by binding its receptor CXCR3, it directly recruits cytotoxic T lymphocytes and NK cells to the liver, promoting hepatocyte apoptosis and driving inflammation. This chemokine also activates hepatic stellate cells (HSCs), stimulating fibrogenesis and disease progression in conditions ranging from viral hepatitis to metabolic steatotic liver disease (MASLD) and cirrhosis. Consequently, IP-10 has emerged as a sensitive biomarker for liver inflammation and fibrosis. This review highlights these mechanistic insights, linking CXCL10's causal roles to its diagnostic, prognostic, and therapeutic potential. We examine its utility in early detection, risk stratification, and targeted therapies to modulate immune responses and reduce fibrosis. We also discuss innovative applications in personalized medicine and precision diagnostics that offer new opportunities to improve outcomes in viral hepatitis and other liver diseases. By integrating mechanistic understanding with clinical implications, this work clarifies the multifaceted role of CXCL10 and identifies future research directions to optimize its therapeutic and diagnostic applications.