A possible role for NKT-like cells in patients with chronic hepatitis B during telbivudine treatment.
Natural killer T-like (NKT-like) cells are a source of different pro-inflammatory cytokines and therefore may be involved in inflammatory processes. However, little is known about NKT-like cells during antiviral therapy. In this study, we observed significantly higher numbers of CD3(+)CD56(+) cells in patients with chronic hepatitis B (CHB) than healthy controls. Importantly, CD3(+)CD56(+) NKT-like cells markedly decreased during telbivudine treatment in patients with CHB, and a positive correlation between NKT-like cell frequency and the serum HBV DNA level was observed during early antiviral therapy. Interestingly, NKT-like cell frequency significantly reduced in well-responders at week 12 of telbivudine therapy compared to baseline, but did not significantly change in non-responders after treatment. Previous studies have shown that interleukin (IL)-17 plays a role in the pathogenesis of CHB. Serum IL-17 levels reduced significantly during early antiviral therapy, however, interferon (IFN)-γ, IL-6 and tumor necrosis factor (TNF)-α levels did not change significantly. A positive correlation was observed between the NKT-like cell frequency and serum IL-17 level in CHB patients, and NKT-like cells isolated from patients with CHB secreted substantial amounts of IL-17 in vitro. These results suggest that the NKT-like cell frequency may be one of useful immunologic marker for evaluating the efficacy of anti-HBV therapy, and that NKT-like cells are also an important source of IL-17 (in addition to conventional T cells) in patients with CHB.
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China. Electronic address: diaohy@zju.edu.cn.
Hongyan
H
Diao
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China.
Jianqin
J
He
The College of Education, Zhejiang University, Hangzhou, Zhejiang 310003, China.
Qishi
Q
Zheng
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China.
Jianing
J
Chen
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China.
Guangying
G
Cui
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China.
Yingfeng
Y
Wei
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, China.
Ping
P
Ye
Department of Microbiology, School of Medicine, Hokkaido University, Sapporo 0600815, Japan.
Masashi
M
Kohanawa
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China. Electronic address: ljli@zju.edu.cn.
Lanjuan
L
Li
D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D005260:Female; D006515:Hepatitis B virus / Q000276:immunology*; D019694:Hepatitis B, Chronic / Q000188:drug therapy* / Q000276:immunology* / Q000821:virology; D006801:Humans; D016130:Immunophenotyping; D020381:Interleukin-17 / Q000096:biosynthesis; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D055611:Natural Killer T-Cells / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D000077712:Telbivudine; D013936:Thymidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D016896:Treatment Outcome; D019562:Viral Load; D055815:Young Adult
D000998:Antiviral Agents; D020381:Interleukin-17; D000077712:Telbivudine; D013936:Thymidine
Chronic hepatitis B; IL-17; NKT-like cells; Telbivudine treatment