ArticleFrontiers in pharmacology2018
Interleukin-35 Attenuates D-Galactosamine/Lipopolysaccharide-Induced Liver Injury via Enhancing Interleukin-10 Production in Kupffer Cells.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 29 citations in OpenAlex.
- The Multifaceted Role of Regulatory T Cells in Sepsis: Mechanisms, Heterogeneity, and Pathogen-Tailored Therapies.International journal of molecular sciences · 2025Review
- The recombinant IL-35 and anti-Ebi3 antibody administration before implantation modulate immune regulation and fetal outcomes in an abortion-prone mouse model.Frontiers in immunology · 2025Article
- Plasma Interleukin-35 Levels Predict the Prognosis in Patients with HBV-Related Acute-on-Chronic Liver Failure.Viruses · 2024Article
- Experimental Yellow Fever in Squirrel Monkey: Characterization of Liver In Situ Immune Response.Viruses · 2023Article
- Memory Impairment, Pro-Inflammatory Host Response and Brain Histopathologic Severity in Rats Infected withPathogens (Basel, Switzerland) · 2022Article
- Interleukin-35 has a tumor-promoting role in hepatocellular carcinoma.Clinical and experimental immunology · 2021Article
- Interleukin-35 Suppresses CD8Digestive diseases and sciences · 2020Article
- Article
- The Role of IL-35 in the Pathophysiological Processes of Liver Disease.Frontiers in pharmacology · 2020Review
- Crosstalk network among multiple inflammatory mediators in liver fibrosis.World journal of gastroenterology · 2019Review
- Role of macrophages in experimental liver injury and repair in mice.Experimental and therapeutic medicine · 2019Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL) -35 is an anti-inflammatory cytokine which exerts various beneficial effects on autoimmune diseases. However, whether IL-35 plays a role in endotoxin induced hepatitis demands clarification. This study aims to reveal the effect and mechanism of IL-35 on endotoxin induced liver injury. Acute hepatic injury was induced by D-galactosamine (D-GalN, 400 mg/kg) and lipopolysaccharide (LPS, 5 μg/kg) administration in mice. IL-35 treatment ameliorated D-GalN/LPS induced liver injury in a dose dependent manner as shown by histological examination, ALT determination and Caspase-3 activity assay. It also reduced production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-α, IL-1β, and IL-6, and increased production of anti-inflammatory cytokines, IL-4, IL-10, and transforming growth factor (TGF)-β. This hepato-protective effect was proved mainly mediated by Kupffer cells (KC) via gadolinium chloride depletion and cell adoptive transfer experiment. In addition, IL-35 emolliated the cytotoxicity of LPS-triggered KCs to hepatocytes, suppressed nitric oxide (NO) and TNF-α production, and elevated IL-10 production in LPS stimulated KCs. Furthermore, IL-35 could not exert hepato-protective effect in IL-10-deficient mice
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