NDLI: Inhibition of SATB1 expression in regulatory T cells contributes to hepatitis B virus-related chronic liver inflammation.

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Inhibition of SATB1 expression in regulatory T cells contributes to hepatitis B virus-related chronic liver inflammation.

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Inhibition of SATB1 expression in regulatory T cells contributes to hepatitis B virus-related chronic liver inflammation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dong, Yue-Jiao Zhu, Qiao-Yun Kong, Hai-Shen Li, Xue-Fen Ni, Qin Tian, Li Chen, Yu Wang, Yi-Yin
Description	Author Affiliation: Li XF ( State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.); Tian L ( Department of Laboratory Medicine, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.); Wang YY ( Department of Laboratory Medicine, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.); Kong HS ( State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.); Dong YJ ( Department of Laboratory Medicine, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.); Zhu QY ( Department of Laboratory Medicine, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.); Ni Q ( State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.); Chen Y ( State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.)
Abstract	Regulatory T cells (Tregs) contribute to the pathogenesis of chronic hepatitis B (CHB). Special AT-rich sequence-binding protein 1 (SATB1) may be a key component of this process. In the present study, Tregs and conventional T cells (Tconvs) were isolated by magnetic cell sorting of peripheral blood from CHB patients (n=57), individuals with resolved hepatitis B virus (HBV) infections (n=15), and healthy controls (n=29). SATB1 expression was studied by reverse transcription-quantitative PCR, flow cytometry and immunofluorescence microscopy, and the correlation of SATB1 expression to the expression of liver inflammation serum markers and the HBV DNA load was assessed. CHB patients showed significantly reduced SATB1 expression in Tregs than healthy controls and individuals with resolved HBV infections. Moreover, SATB1 expression in Tregs was significantly lower than in Tconvs of patients with chronic HBV infection. Serum HBV DNA and liver inflammation markers were inversely correlated to the SATB1 mRNA level in Tregs. Antiviral treatment was accompanied by increased expression of the SATB1 gene in Tregs. Thus, Tregs from CHB patients have reduced levels of SATB1, which is resolved with antiviral therapy. Inhibition of SATB1 expression may impair the hepatic inflammatory response and contribute to HBV persistence.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	1
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-01-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Gene Expression Hepatitis B Virus Hepatitis B, Chronic Genetics Immunology Matrix Attachment Region Binding Proteins T-lymphocytes, Regulatory Metabolism Antiviral Agents Pharmacology Therapeutic Use Case-control Studies Gene Expression Regulation Drug Effects Drug Therapy Virology Immunophenotyping Interferon-alpha Liver Function Tests Polyethylene Glycols Rna, Messenger Recombinant Proteins Viral Load Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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