ReviewHepatology (Baltimore, Md.)2021
The Emerging Role of B Cells in the Pathogenesis of NAFLD.
Review in Hepatology (Baltimore, Md.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
76 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.
- Therapeutic potential and mechanisms of flavonoids from Citrus grandis 'Tomentosa' in metabolic dysfunction-associated steatotic liver disease: a focus on immune-inflammatory signaling pathways.Frontiers in pharmacology · 2026Pooled it
- GDF15 in Liver Fibrosis: Molecular Mechanisms, Immunoregulatory Functions, and Therapeutic Potential.Biomolecules · 2026Review
- Mechanisms and therapeutic insights into MASH-associated fibrosis.Trends in endocrinology and metabolism: TEM · 2026Review
- Mechanism and therapeutic prospects of adipose tissue B lymphocytes in obesity and obesity‑associated metabolic diseases (Review).Molecular medicine reports · 2026Review
- Incretin and Glucagon Signalling in MASLD and MASH: Integrating Metabolic Pathways With Disease Progression.Diabetes, obesity & metabolism · 2026Review
- Crosstalk between SPP1+ macrophages and ITGA5+ fibroblasts promotes hepatocellular carcinoma metastasis.Hepatology communications · 2026Article
- Single-cell transcriptomic landscape of intrahepatic B Cells in MASH.BMC gastroenterology · 2026Article
- Immune crosstalk in metabolic dysfunction-associated steatotic liver disease: interactions between innate and adaptive immunity.Frontiers in immunology · 2026Review
- Editorial: Adaptive immune regulation of non-alcoholic steatohepatitis (NASH).Frontiers in immunology · 2026Article
- Pathogenesis of metabolic dysfunction-associated steatotic liver disease and donor liver damage.iLIVER · 2025Review
- Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025Review
- Constructing biomimetic microenvironments for liver regeneration.Journal of nanobiotechnology · 2025Review
- Sterile inflammation in MASH: emerging role of extracellular RNA and therapeutic strategies.npj metabolic health and disease · 2025Review
- Immune microenvironment in hepatocellular carcinoma: from pathogenesis to immunotherapy.Cellular & molecular immunology · 2025Review
- Autoimmunity in MASLD: Focus on autoantibodies, anti-apolipoprotein A1 IgG and G protein-coupled receptors.European journal of clinical investigation · 2025Review
- Article
- Inflammation in MASLD progression and cancer.JHEP reports : innovation in hepatology · 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
- Cell-Type Deconvolution Reveals Dynamic Changes in MASLD.Liver international communications · 2025Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
NAFLD is one of the leading causes of abnormal liver function worldwide. NAFLD refers to a group of liver conditions ranging from nonalcoholic fatty liver to NASH, which involves inflammation, hepatocellular damage, and fibrosis. Triggering of inflammation in NASH is a key event in the progression of the disease, and identifying the factors that initiate or dysregulate this process is needed to develop strategies for its prevention or treatment. B cells have been implicated in several autoimmune and inflammatory diseases. However, their role in the pathogenesis of NAFLD and NASH is less clear. This review discusses the emerging evidence implicating intrahepatic B cells in the progression of NAFLD. We highlight the potential mechanisms of B-cell activation during NAFLD, such as increased hepatic expression of B-cell-activating factor, augmented oxidative stress, and translocation of gut-derived microbial products. We discuss the possible effector functions by which B cells promote NAFLD, including the production of proinflammatory cytokines and regulation of intrahepatic T cells and macrophages. Finally, we highlight the role of regulatory and IgA
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Registered trials
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.