ArticleHepatology international2013
Maturation defective myeloid dendritic cells in nonalcoholic fatty liver disease patients release inflammatory cytokines in response to endotoxin.
Article in Hepatology international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Dynamic immune landscape of NAFLD highlights pDCs as predictive biomarkers for disease progression.Frontiers in immunology · 2026Article
- PLA 3D Printing as a Straightforward and Versatile Fabrication Method for PDMS Molds.Polymers · 2023Article
- The Riddle of Nonalcoholic Fatty Liver Disease: Progression From Nonalcoholic Fatty Liver to Nonalcoholic Steatohepatitis.Journal of clinical and experimental hepatology · 2015Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeNonalcoholic fatty liver disease (NAFLD) is characterized by the presence of elevated circulating endotoxin levels. The continuous presence of endotoxin might be responsible for inducing activation of the innate immune system resulting in chronic sub-clinical inflammation. This study examines the status of dendritic cells (DCs), an important component of innate immune system, in patients with NAFLD.
methodsEffect of lipopolysaccharide (LPS) stimulation on maturation and activation of monocyte derived dendritic cells (mo-DCs) was evaluated in ten patients with NAFLD using flow cytometry, endocytosis assay, cytokine assay and mixed leukocyte reaction.
resultsAlthough the frequency of mo-DCs in NAFLD patients was similar to that of healthy controls, there was no upregulation in levels of HLA-DR, CD83, CD80 and CD86 on their surface in response to LPS stimulation ex vivo. Although the mo-DC from patients had higher endocytosing and lower allostimulatory capacities as compared to healthy controls indicating maturation defects yet they secreted significantly high amount of TNF-α and IL-6 suggesting higher activation state.
conclusionsOur results indicate that DCs in patients with NAFLD exhibit immature yet functionally activated phenotype in response to LPS stimulation as they secrete inflammatory cytokines which further contribute in exacerbating the symptoms. Inefficient antigen presentation in these patients might add another parameter while looking at the severity of disease.
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