KCTD9 contributes to liver injury through NK cell activation during hepatitis B virus-induced acute-on-chronic liver failure

详细信息    查看全文

• 作者：Tao Chen^a ; Lin Zhu^a ; Yaoyong Zhou^a ; ¹ ; Bin Pi^a ; Xiaojuan Liu^a ; Guohong Deng^b ; Rong Zhang^b ; Yuming Wang^b ; Zeguang Wu^a ; Meifang Han^a ; Xiaoping Luo^c ; ^{xpluo888@sina.com} ; Qin Ning^a ; ^{qning66@yahoo.com.cn}
• 关键词：KCTD ; potassium channel tetramerisation domain containing ; KCTD9 ; potassium channel tetramerisation domain containing 9 ; hKCTD9 ; human KCTD9 ; CHB ; chronic hepatitis B ; HBV-ACLF ; HBV induced acute-on-chronic liver failure ; PBMC ; peripheral blood mononuclea
• 刊名：Clinical Immunology
• 出版年：2013
• 出版时间：March, 2013
• 年：2013
• 卷：146
• 期：3
• 页码：207-216
• 全文大小：1240 K

文摘

We explored the expression of a newly identified potassium channel tetramerisation domain containing 9 (KCTD9) protein in 113 blood and 81 liver samples, from patients with mild chronic hepatitis B (CHB) or HBV-induced acute-on-chronic liver failure (HBV-ACLF). KCTD9 was highly expressed in peripheral and hepatic NK cells from HBV-ACLF patients compared with mild CHB patients, and this correlated positively with the severity of liver injury. The role of KCTD9 was further investigated in NK92 cells in vitro. KCTD9 overexpressed NK92 cells exhibited a marked increase in CD69 expression, cytotoxicity, IFN-¦Ã secretion and a significant decrease in NKG2A receptor expression. Inhibition of KCTD9 by shRNA resulted in reduced cytotoxic function. These results suggest the involvement of KCTD9 in NK cell activation and provide additional insight into a potential therapeutic target for molecular manipulation for HBV-ACLF patients.