Background C–X–C motif chemokine ligand 13 (CXCL13) is a critical chemokine for lymphoid organization and immune cell migration during hepatitis B virus (HBV) infection. This systematic review assessed the function of CXCL13 in HBV immunoregulation, pathogenesis, genetic susceptibility, and treatment outcome. Methods We systematically searched five databases, including PubMed, Scopus, Web of Science, and Google Scholar, to identify studies reporting on CXCL13 expression, genetic variants, and clinical outcomes in the context of HBV infection. Thirteen qualified studies were identified and assessed using standard quality appraisal instruments. Results Data consistently supported the role of CXCL13 in recruiting CXCR5 T and B cells, conditioning germinal center–like reaction(s) as well as antiviral immune responses. Elevated serum CXCL13 levels correlated with better virological response, higher HBsAg clearance, and more favorable response to PegIFNα and nucleos(t)ide analogs. On the other hand, downregulation of CXCL13 was associated with immune tolerance, resistance failure, and disease persistence. Genetically, these polymorphic sites, such as rs355687 and rs76084459, have been associated with vaccine response, the possibility of transplacental transmission, and outcomes of antiviral therapy. Conclusion CXCL13 is a key immunomodulatory factor in HBV infection and represents an excellent candidate predictive biomarker for treatment response and disease course. Prospective multicenter studies and laboratory research are needed to confirm its usefulness in clinical trials and to investigate therapeutic strategies targeting CXCL13.
Bello et al. (Thu,) studied this question.