ArticleHepatology (Baltimore, Md.)2015
Liver fibrosis occurs through dysregulation of MyD88-dependent innate B-cell activity.
Article in Hepatology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 95 citations in OpenAlex.
- GDF15 in Liver Fibrosis: Molecular Mechanisms, Immunoregulatory Functions, and Therapeutic Potential.Biomolecules · 2026Review
- The immunometabolic nature of MASH: framing immune cells within metabolic dysfunction.Frontiers in immunology · 2026Review
- Hepatic mitochondrial signaling as a systemic hub: inter-organ communication networks in aging and aging-related diseases.Frontiers in cell and developmental biology · 2026Review
- Immune cells in liver injury: from pathogenic mechanisms to immunotherapy.Frontiers in immunology · 2026Review
- Nuclear localization of Toll/interleukin-1 receptor domain-containing adaptor protein reveals a previously unrecognized role in hepatic stellate cell activation.Frontiers in immunology · 2026Article
- Immune cell fibrotic plasticity: mesenchymal-like reprogramming of macrophages, neutrophils and T cells.Frontiers in immunology · 2026Review
- Dissecting the mechanisms of MASLD fibrosis in the era of single-cell and spatial omics.The Journal of clinical investigation · 2025Review
- The role of immune cells in cirrhosis: evidence from a two-sample Mendelian randomization study.Scientific reports · 2025Article
- Distinct Biomarker Profiles of B-Cell Activation in Metabolic and Viral Hepatic Fibrosis.International journal of molecular sciences · 2025Article
- Review
- Exploring Proteomic Alterations in Intellectual Disability: Insights from Hyperlipidemia and Hyperphosphatasia Subgroups.Neuromolecular medicine · 2025Article
- Prognostic assessment of early-stage liver cirrhosis induced by HCV using an integrated model of CX3CR1-associated immune infiltration genes.Scientific reports · 2025Article
- Immunotherapy resistance in MASLD-related hepatocellular carcinoma: special immune microenvironment and gut microbiota.International journal of biological sciences · 2025Review
- Dynamic crosstalk between HSCs and liver microenvironment: multicellular interactions in the regulation of liver fibrosis.Frontiers in cell and developmental biology · 2025Review
- Article
- Oral Health and "Modern" Digestive Diseases: Pathophysiologic and Etiologic Factors.Biomedicines · 2024Review
- Developmental Programming of the Fetal Immune System by Maternal Western-Style Diet: Mechanisms and Implications for Disease Pathways in the Offspring.International journal of molecular sciences · 2024Review
- Molecular Genealogy of Metabolic-associated Hepatocellular Carcinoma.Seminars in liver disease · 2024Review
- Immunopathogenesis of liver fibrosis in steatotic liver disease.Clinical and molecular hepatology · 2024Article
- Exploration of a hypoxia-immune-related microenvironment gene signature and prediction model for hepatitis C-induced early-stage fibrosis.Journal of translational medicine · 2024Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
unlabelledChronic liver disease mediated by activation of hepatic stellate cells (HSCs) leads to liver fibrosis. Here, we postulated that the immune regulatory properties of HSCs might promote the profibrogenic activity of B cells. Fibrosis is completely attenuated in carbon tetrachloride-treated, B cell-deficient µMT mice, showing that B cells are required. The retinoic acid produced by HSCs augmented B-cell survival, plasma cell marker CD138 expression, and immunoglobulin G production. These activities were reversed following addition of the retinoic acid inhibitor LE540. Transcriptional profiling of fibrotic liver B cells revealed increased expression of genes related to activation of nuclear factor κ light chain enhancer of activated B cells, proinflammatory cytokine production, and CD40 signaling, suggesting that these B cells are activated and may be acting as inflammatory cells. Biological validation experiments also revealed increased activation (CD44 and CD86 expression), constitutive immunoglobulin G production, and secretion of the proinflammatory cytokines tumor necrosis factor-α, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1α. Likewise, targeted deletion of B-cell-intrinsic myeloid differentiation primary response gene 88 signaling, an innate adaptor with involvement in retinoic acid signaling, resulted in reduced infiltration of migratory CD11c(+) dendritic cells and Ly6C(++) monocytes and, hence, reduced liver pathology.
conclusionLiver fibrosis occurs through a mechanism of HSC-mediated augmentation of innate B-cell activity. These findings highlight B cells as important "first responders" of the intrahepatic immune environment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.