Transfusion of autologous cytokine-induced killer cells inhibits viral replication in patients with chronic hepatitis B virus infection

被引:51
作者
Shi, Ming
Fu, Junliang
Shi, Feng
Zhang, Bin
Tang, Zirong
Jin, Lei
Fan, Zhenping [2 ]
Zhang, Zheng
Chen, Liming [2 ]
Wang, Huifeng [2 ]
Lau, George K. K. [3 ]
Wang, Fu-Sheng [1 ,2 ]
机构
[1] Beijing 302 Hosp, Res Ctr Biol Therapy, Beijing Inst Infect Dis, Beijing 100039, Peoples R China
[2] Beijing 302 Hosp, Clin Dept 6, Beijing 100039, Peoples R China
[3] Univ Hong Kong, Queen Mary Hosp, Dept Med, Hong Kong, Hong Kong, Peoples R China
基金
中国国家自然科学基金;
关键词
Cytokine-induced killer cell; Hepatitis B virus; Chronic hepatitis B; Safety; Efficacy; REGULATORY T-CELLS; HEPATOCELLULAR-CARCINOMA PATIENTS; BONE-MARROW-TRANSPLANTATION; SURFACE-ANTIGEN; IN-VIVO; LYMPHOCYTE RESPONSE; IMMUNE-RESPONSE; DENDRITIC CELLS; UP-REGULATION; THERAPY;
D O I
10.1016/j.clim.2009.03.001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Adoptive immune transfer plays an important rote in clearance of hepatitis B virus (HBV) in chronic hepatitis B (CHB) patients. However, it is unclear whether cytokine-induced killer (CIK) cells could suppress HBV replication in CHB patients, especially if drug resistance develops. In this study, functional CIK cells were efficiently generated from 21 CHB patients and were transfused in an autologous manner. We found that CIK cells from the CHB patients displayed substantial proliferation and function. Administration of the CIK cells closely correlated with the decrease in the serum HBV toad and improvement in liver function in some patients. The virological response rate in patients with baseline serum alanine aminotransferase (ALT) levels of >40 U/L was higher than that in patients with baseline serum ALT levels of <= 40 U/L. Moreover, patients who had HBeAg loss or showed seroconversion generally had baseline serum ALT levels of >40 U/L. No serious side effects were observed. This protocol represents an alternative immune therapeutic strategy for the disease. (C) 2009 Published by Elsevier Inc.
引用
收藏
页码:43 / 54
页数:12
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