原创力文档tgf-β1 down-regulation of nkg2ddap10 and 2b4sap expression on human nk cells contributes to hbv persistencetgf-β1 nkg2ddap10和2 b4sap表达的下调对人类nk细胞导致乙肝病毒的持久性.pdfVIP
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tgf-β1 down-regulation of nkg2ddap10 and 2b4sap expression on human nk cells contributes to hbv persistencetgf-β1 nkg2ddap10和2 b4sap表达的下调对人类nk细胞导致乙肝病毒的持久性
TGF-b1 Down-Regulation of NKG2D/DAP10 and 2B4/SAP
Expression on Human NK Cells Contributes to HBV
Persistence
1 1,2 3 1 1,2 1,2 1,2
Cheng Sun , Binqing Fu , Yufeng Gao , Xiaofeng Liao , Rui Sun , Zhigang Tian *, Haiming Wei *
1 Institute of Immunology, School of Life Sciences, University of Science and Technology of China, Hefei, China, 2 Hefei National Laboratory for Physical Sciences at
Microscale, University of Science and Technology of China, Hefei, China, 3 Department of Liver Diseases of the Second Affiliated Hospital of Anhui Medical University,
Hefei, China
Abstract
The mechanism underlying persistent hepatitis B virus (HBV) infection remains unclear. We investigated the role of innate
immune responses to persistent HBV infection in 154 HBV-infected patients and 95 healthy controls. The expression of
NKG2D- and 2B4-activating receptors on NK cells was significantly decreased, and moreover, the expression of DAP10 and
SAP, the intracellular adaptor proteins of NKG2D and 2B4 (respectively), were lower, which then impaired NK cell-mediated
cytotoxic capacity and interferon-c production. Higher concentrations of transforming growth factor-beta 1 (TGF-b1) were
found in sera from persistently infected HBV patients. TGF-b1 down-regulated the expression of NKG2D and 2B4 on NK cells
in our in vitro study, leading to an impairment of their effector functions. Anti-TGF-b1 antibodies could restore the
expression of NKG2D and 2B4 on NK cells in vitro. Furthermore, TGF-b1 induced cell-cycle arrest in NK cells by up-regulating
the expression of p15 and p21 in NK cells from immunotolerant (IT) patients. We conclude that TGF-b1 may reduce the
expre
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