ArticleDigestive diseases and sciences2014
Chemokine-chemokine receptor CCL2-CCR2 and CX3CL1-CX3CR1 axis may play a role in the aggravated inflammation in primary biliary cirrhosis.
Article in Digestive diseases and sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 75 citations in OpenAlex.
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- Cellular senescence in liver diseases: From molecular drivers to therapeutic targeting.Journal of hepatology · 2026Review
- CX3CL1/CX3CR1 axis in liver disease: context-dependent roles and balance.Frontiers in immunology · 2026Review
- Dietary Lauric Acid Suppresses Inflammation, Cholestasis, Hepatocyte Injury, and Senescence in 3,5-Diethoxycarbonyl-1,4-Dihydrocollidine-induced Inflammatory Cholangiopathy.Cellular and molecular gastroenterology and hepatology · 2026Article
- Cellular senescence mediates doxorubicin chemotherapy-induced vascular endothelial dysfunction: translational evidence of prevention with senolytic treatment.American journal of physiology. Heart and circulatory physiology · 2025Article
- New perspectives in the treatment of liver cirrhosis: targeting macrophage regulatory mechanisms.Journal of translational medicine · 2025Review
- Identification of Crosstalk Genes Between Primary Sjögren's Syndrome and Primary Biliary Cirrhosis by Transcriptome Analysis.Digestive diseases and sciences · 2025Article
- Clinical management of autoimmune liver diseases: juncture, opportunities, and challenges ahead.Immunologic research · 2025Review
- Common pathological mechanisms and therapeutic strategies in primary Sjogren's syndrome and primary biliary cholangitis: from tissue immune microenvironment to targeted therapy.Frontiers in immunology · 2025Review
- Mitochondria at the Crossroads of Cholestatic Liver Injury: Targeting Novel Therapeutic Avenues.Journal of clinical and translational hepatology · 2024Review
- Mechanism-based target therapy in primary biliary cholangitis: opportunities before liver cirrhosis?Frontiers in immunology · 2023Review
- CX3CR1 deficiency exacerbates immune-mediated hepatitis by increasing NF-κB-mediated cytokine production in macrophage and T cell.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Identification of Pathogenic Immune Cell Subsets Associated With Checkpoint Inhibitor-Induced Myocarditis.Circulation · 2022Article
- Primary Biliary Cholangitis and Primary Sclerosing Cholangitis: Current Knowledge of Pathogenesis and Therapeutics.Biomedicines · 2022Review
- Vascular Protective Effects ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Inhibition of Secretin/Secretin Receptor Axis Ameliorates NAFLD Phenotypes.Hepatology (Baltimore, Md.) · 2021Article
- Interferon-induced protein with tetratricopeptide repeats 3 may be a key factor in primary biliary cholangitis.Scientific reports · 2021Article
- Association of CX3CL1 and CX3CR1 Expression with Liver Fibrosis in a Mouse Model of Schistosomiasis.Current medical science · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsSenescent cells can alter local tissue environments by secretion of various senescence-associated secretory phenotypes (SASP), such as cytokines and chemokines. Given senescent biliary epithelial cells (BECs) in damaged small bile ducts in primary biliary cirrhosis (PBC) show increased expression of chemokines CCL2 and CX3CL1 as SASP, we further examined an involvement of CCL2/CCR2 and CX3CL1/CX3CR1 systems in the pathogenesis of PBC.
methodsWe examined immunohistochemically the expression of CCR2, CX3CR1, CCL2 and CX3CL1 in livers taken from the patients with PBC (n = 45) and control livers (n = 78), such as chronic viral hepatitis (CVH; n = 39). CCR2 or CX3CR1-expressing cells were characterized by double immunofluorescence with CD3, CD4, CD8, CD56 or CD68.
resultsCCR2 is expressed in round cells, epithelioid cells and dendritic cells and most CCR2-positive cells were CD68-positive. Infiltration of CCR2-positive cells in the intraepithelial layer or around small bile ducts was significantly more extensive in PBC than CVH and normal liver (p < 0.05) and was significantly correlated with the expression of CCL2 in BECs (p < 0.01). Most CX3CR1-expressing inflammatory cells were CD3-positive T cells (CD8 > CD4). Infiltration of CX3CR1-positive cells in the intraepithelial layer and around small bile ducts was significantly more extensive in PBC than control livers (p < 0.05) and was significantly correlated with the expression of CX3CL1 in BECs (p < 0.05).
conclusionCCL2 and CX3CL1 produced by senescent BECs may promote infiltration of corresponding CCR2 and CX3CR1-expressing cells and further aggravate inflammation in bile duct lesion in PBC.
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