ArticleHepatology (Baltimore, Md.)2010
CX3CL1 (fractalkine): a signpost for biliary inflammation in primary biliary cirrhosis.
Article in Hepatology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
What it found
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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
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.
- A regulatory variant at 19p13.3 is associated with primary biliary cholangitis risk and ARID3A expression.Nature communications · 2023Pooled it
- Primary Biliary Cholangitis Pathogenesis: A Pathophysiology-Based Narrative Review.International journal of molecular sciences · 2026Review
- CX3CL1/CX3CR1 axis in liver disease: context-dependent roles and balance.Frontiers in immunology · 2026Review
- The Treatment of Primary Biliary Cholangitis: Time for Personalized Medicine.Clinical reviews in allergy & immunology · 2025Review
- CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis.International journal of molecular sciences · 2024Review
- Targeting Gut Microbiota for the Treatment of Primary Biliary Cholangitis: From Bench to Bedside.Journal of clinical and translational hepatology · 2023Review
- Article
- Primary Biliary Cholangitis and Primary Sclerosing Cholangitis: Current Knowledge of Pathogenesis and Therapeutics.Biomedicines · 2022Review
- The gut-liver axis in cholangiopathies: focus on bile acid based pharmacological treatment.Current opinion in gastroenterology · 2022Review
- APASL clinical practice guidance: the diagnosis and management of patients with primary biliary cholangitis.Hepatology international · 2022Article
- Current understanding of primary biliary cholangitis.Clinical and molecular hepatology · 2021Review
- Interleukin 23 Produced by Hepatic Monocyte-Derived Macrophages Is Essential for the Development of Murine Primary Biliary Cholangitis.Frontiers in immunology · 2021Article
- Galectin-3 in Inflammasome Activation and Primary Biliary Cholangitis Development.International journal of molecular sciences · 2020Review
- Primary biliary cholangitis: pathogenesis and therapeutic opportunities.Nature reviews. Gastroenterology & hepatology · 2020Review
- RANK/RANKL Acts as a Protective Factor by Targeting Cholangiocytes in Primary Biliary Cholangitis.Digestive diseases and sciences · 2020Article
- Association between serum ficolin-1 level and disease progression in primary biliary cholangitis.PloS one · 2020Article
- Immune Cell Trafficking to the Liver.Transplantation · 2019Review
- Therapeutic and immunological interventions in primary biliary cholangitis: from mouse models to humans.Archives of medical science : AMS · 2018Article
- Update on New Drugs and Those in Development for the Treatment of Primary Biliary Cholangitis.Gastroenterology & hepatology · 2018Article
- Tissue-specific Role of CXImmune network · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
Abstract
unlabelledImprovements in the treatment of primary biliary cirrhosis (PBC) may depend upon dissection of mechanisms that determine recruitment of mononuclear cells to intralobular bile ducts, including the role of the chemokine-adhesion molecule CX3CL1 (fractalkine). We submit that there are unique interactions between intrahepatic biliary epithelial cells (BECs), endothelial cells (ECs), liver sinusoidal endothelial cells (LSECs), and liver-infiltrating mononuclear cells (LMCs), and that such interactions will in part dictate the biliary-specific inflammatory response. To address this, we studied fresh explanted livers from pretransplantation patients with PBC and with inflammatory liver disease due to viral infection (disease controls) and biopsy material from patients with a discrete liver tumor (normal controls). Using this clinical material, we isolated and stimulated BECs, ECs, LSECs, and LMCs with a panel of Toll-like receptor ligands. We also studied the interactions of these cell populations with LMCs with respect to adhesion capability and production of tumor necrosis factor alpha (TNF-alpha). Finally, we used fresh biopsy samples to evaluate mononuclear cells around intrahepatic biliary ductules using monoclonal antibodies specific to CD68 or CD154, markers for monocytes/macrophages, and activated T cells, respectively.
conclusionThere are common properties of ECs, LSECs, and BECs, whether derived from PBC or viral hepatitis, but there are also significant differences, particularly in the potential in PBC for LMCs to adhere to ECs and BECs and to produce TNF-alpha; such properties were associated with augmented CX3CL1 production by BEC from PBC liver. The processes defined herein suggest potential novel biotherapies for biliary specific inflammation.
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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.