ArticleClinical and experimental medicine2026
A genomic and transcriptomic integration study of CCL19-driven macrophage-immune crosstalk in chronic hepatitis B.
Article in Clinical and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Chronic hepatitis B (CHB) progression features stage-dependent immune dysfunction, transitioning from high viremia in immune-tolerant phases to persistent liver injury during immune activity. While inflammatory mediators facilitate hepatitis B virus (HBV) persistence and hepatocyte damage, their causal orchestration remains undefined. This multi-omics investigation systematically identifies inflammation-related therapeutic targets through causal inference analysis of CHB pathogenesis. We conducted two-sample Mendelian randomization (TSMR) analysis to investigate causal associations with circulatory inflammatory mediators. Subsequent integrative multi-omics investigations incorporated single-cell transcriptomic profiling (GSE186343 and GSE182159) and bulk tissue sequencing data (GSE65359 and GSE83148). Single-cell data processing involved Seurat pipelines with Harmony batch correction. Transcriptomic alterations were systematically characterized using limma-based differential analysis coupled with CIBERSORT-mediated immune composition deconvolution. Molecular networks were established through pySCENIC transcriptional regulation modeling, cellular differentiation patterns were resolved via Monocle2 trajectory inference, and ligand-receptor dynamics were examined using CellChat/NicheNet frameworks. Therapeutic compound identification was achieved through computational screening of CMAP pharmacogenomic signatures. This investigation applied TSMR to pinpoint CCL19 as a principal mediator among 91 circulatory inflammatory proteins exhibiting causal positivity in CHB pathogenesis. Mechanistic multi-omics integration delineated its immunomodulatory pathways. Genomic epidemiology demonstrated that heightened circulating CCL19 concentrations substantially elevate hepatitis B viral susceptibility. Single-cell resolution profiling revealed CCL19 spatial enrichment specifically within antigen-presenting macrophage clusters (M4 phenotype) in CHB hepatic microenvironments. Functional coordination was observed with pro-inflammatory cytotoxic macrophage populations (M3 phenotype) through IFNG and HLA signaling crosstalk, simultaneously potentiating antiviral defense mechanisms and inflammatory tissue damage. Subsequently, we postulated a transcriptional regulatory cascade involving RB1, MEF2A, and SEMA4A that may control CCL19 expression. The investigation demonstrated a dysregulation in the balance of macrophage and T cell subsets among CHB patients, while pinpointing CCL19 as a critical macrophage-derived biomarker. This chemokine’s upregulated expression may exhibit significant correlations with amplified chemotactic signaling and engagement of the antigen processing/presentation cascade.
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