ArticleJournal of biomedical science2018
The human C-type lectin 18 is a potential biomarker in patients with chronic hepatitis B virus infection.
Article in Journal of biomedical science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- CLEC18A interacts with sulfated glycosaminoglycans and controls clear cell renal cell carcinoma progression.The FEBS journal · 2026Article
- Characterization of the genetic variation and evolutionary divergence of the CLEC18 family.Journal of biomedical science · 2024Article
- The development of radioresistant oral squamous carcinoma cell lines and identification of radiotherapy-related biomarkers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- CLEC18A Impairs Phagocytosis by Reducing FcγRIIA Expression and Arresting Autophagosome-Lysosome Fusion.Microbiology spectrum · 2023Article
- Human rs75776403 polymorphism links differential phenotypic and clinical outcomes to a CLEC18A p.T151M-driven multiomics.Journal of biomedical science · 2022Article
- Endosomal TLR3 co-receptor CLEC18A enhances host immune response to viral infection.Communications biology · 2021Article
- Transgenic Expression of Human C-Type Lectin Protein CLEC18A Reduces Dengue Virus Type 2 Infectivity inFrontiers in immunology · 2021Article
- Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundHepatitis B virus (HBV) infection is a common disease worldwide and is known to cause liver disease. C-type lectin 18 (CLEC18) is a novel secretory lectin highly expressed in human hepatocytes. Because the liver is the major target of HBV infection, we investigated whether the expression of CLEC18 can be used as a biomarker for HBV infection.
methodsThe expression level of CLEC18 in human liver chimeric mice with/without HBV infection was measured by quantitative real time polymerase chain reaction (qPCR) assay. Baseline plasma CLEC18 levels in 271 treatment-naive patients with chronic hepatitis B (CHB) undergoing nucleos(t)ide analogue (NUC) therapy and 35 healthy donors were measured by enzyme-linked immunosorbent assay, and the relationships to other clinical data were analyzed.
resultsThe expression of CLEC18 was down-regulated in the human liver chimeric mice after HBV infection. Plasma CLEC18 levels were lower in the patients with CHB compared to the healthy donors and positively correlated with HBV DNA and HBsAg levels (P < 0.05). Multivariate Cox proportional hazard regression analysis identified a baseline plasma CLEC18 level of 320-2000 pg/mL to be an independent predictor of HBeAg loss (hazard ratio (HR): 2.077, P = 0.0318), seroconversion (HR: 2.041, P = 0.0445) and virological response (HR: 1.850, P = 0.0184) in 101 HBeAg-positive patients with CHB undergoing NUC therapy.
conclusionsPlasma CLEC18 levels were correlated with the stage of HBV infection and could predict HBeAg loss and seroconversion in the patients with CHB undergoing NUC therapy.
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