Department and Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
Clin Immunol. 2013 Mar;146(3):207-16. doi: 10.1016/j.clim.2012.12.013. Epub 2013 Jan 7.
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-γ 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.
我们研究了一个新鉴定的钾通道四聚化结构域包含 9 蛋白（KCTD9）在 113 份血液和 81 份肝脏样本中的表达情况，这些样本来自患有轻度慢性乙型肝炎（CHB）或乙型肝炎病毒引起的慢加急性肝衰竭（HBV-ACLF）的患者。与轻度 CHB 患者相比，HBV-ACLF 患者外周血和肝 NK 细胞中 KCTD9 的表达水平较高，且与肝损伤的严重程度呈正相关。我们进一步在 NK92 细胞中研究了 KCTD9 的作用。过表达 KCTD9 的 NK92 细胞表现出 CD69 表达、细胞毒性、IFN-γ 分泌显著增加，而 NKG2A 受体表达显著降低。用 shRNA 抑制 KCTD9 会导致细胞毒性功能降低。这些结果表明 KCTD9 参与了 NK 细胞的激活，并为 HBV-ACLF 患者的分子操纵提供了一个潜在的治疗靶点。
