ArticleOncotarget2017
Elevated serum A20 is associated with severity of chronic hepatitis B and A20 inhibits NF-κB-mediated inflammatory response.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- A20 (TNFAIP3) Distinguishes Attack From Remission in Pediatric Patients With Monophasic MOGAD.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Prenatal Stress Increases the Risk of the FPR2-related Dysfunction in the Brain's Resolution of Inflammation: A Study on the Humanized APPCurrent neuropharmacology · 2025Article
- Association of serum A20 levels with stroke-associated pneumonia, early neurological deterioration, and poor neurological prognosis following acute supratentorial intracerebral hemorrhage: a prospective cohort study.Frontiers in neurology · 2025Article
- A prospective cohort study on serum A20 as a prognostic biomarker of aneurysmal subarachnoid hemorrhage.World journal of emergency medicine · 2023Article
- Identification of TNFAIP3 as relapse biomarker and potential therapeutic target for MOG antibody associated diseases.Scientific reports · 2020Article
- Identifying and Characterizing Stress Pathways of Concern for Consumer Safety in Next-Generation Risk Assessment.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Interference of Apoptosis by Hepatitis B Virus.Viruses · 2017Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A20 is a powerful suppressor for inflammatory response. This study aims to determine A20 level in patients with chronic hepatitis B (CHB), and analyze its association with the disease severity. The role of A20 in inflammatory response was further investigated in vivo and in vitro. Our results showed significantly higher A20 in both serum and liver tissues in CHB patients than in health controls. Serum A20 level was positively correlated with ALT, AST and TNF-α. To induce hepatitis with inflammation and liver injury, mice were injected intraperitoneally with D-galactosamine (D-GalN), resulting in rapid increase of A20 in serum and liver tissues. Consistently, HepG2 and Huh-7 cells exposed to Lipopolysaccharide (LPS) or D-GalN were promoted to express A20. Moreover, overexpression or knockdown of A20 inhibited or increased TNF-α secretion separately. A20 significantly reduced pro-inflammatory cytokines expression and down-regulated phospho-IκBα and phospho-p65 in both cells. In conclusion, elevated A20 expression is involved in the severity of CHB, suggesting A20 to be a possible serological biomarker for the disease prognosis. Additionally, the inflammatory response is attenuated by A20 through inhibiting NF-κB activity, which partially contributes to the hepato-protective function of this molecule. Thus, up-regulating A20 might be a potential strategy for preventing the progress of CHB.
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