Elucidating the mechanism of ameliorated liver disease and HBs antigen elimination by nucleos(t)ide analogs in chronic hepatitis B patients

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K19360
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Gastroenterology
• Research Institution: Nagoya City University
• Principal Investigator: HAYASHI Sanae 名古屋市立大学, 大学院医学研究科, 研究員 (10597587)
• Research Collaborator: ISOGAWA Masanori 名古屋市立大学, 大学院医学研究科, 助教 ; TANAKA Yasuhito 名古屋市立大学, 大学院医学研究科, 教授
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: B型肝炎ウイルス / 核酸アナログ / NK細胞 / 肝障害 / 免疫 / 炎症

Outline of Final Research Achievements

In vitro study revealed that CD56bright+TRAIL+ NK cells induce hepatocyte damage in a dose dependent manner, and that HBV infected hepatocytes cocultured with CD56bright+TRAIL+ NK cells promote the chemotaxis of the CD56bright+TRAIL+ NK cells. In an age and gender-matched case study, we analyzed the dynamic changes of an inflammatory cytokine, IP10, in the sera of chronic HBV patients before and after NAs treatment (ETV or TDF). After 12 and 24 weeks of NAs treatment, serum IP10 level was decreased in chronic HBV patients treated with TDF. No significant change was observed in patients treated with ETV.

Free Research Field

医歯薬学