title: Up-regulate HLA class I expression following hepatitis B virus transfection in a hepatocellular carcinoma cell line BEL7405.
abstract: Chronic hepatitis B virus infection is associated with a high risk of developing into hepatocellular carcinoma, while tumor recognition is important during the immune surveillance process that prevents cancer development in humans. The mechanisms of immune evasion and the role of the early immune response in chronic infection caused by hepatitis B virus (HBV) are still unclear. In the present study, 1 copy or 1.2 copies of HBV genome was transfected into a hepatocellular carcinoma cell line BEL7405. RT-PCR, Western blot and flow cytometry analysis were used to evaluate the expression of HLA class I molecules and transporter associated with antigen processing 1 (TAP1). Finally, the cytotoxic activity of natural killer (NK) cells against HBV transfected liver cells was detected by MTT colorimetry method. Following transfection of 1 copy or 1.2 copies of HBV genome, HLA class I expression was up-regulated in BEL7405 cell line in a dose-dependent manner. Furthermore, increased the surface HLA class I expression were caused by enhanced expression of TAP1 at mRNA and protein levels in those transfected cells. Consequently, a significantly down-regulated cytotoxic activity of NK cells against HBV transfected liver cells was observed. These results may demonstrate a way by which HBV avoids recognition by NK cells that might be associated with the establishment of chronic infection and tumor formation.
authors.affiliation: The Key Laboratory of the Ministry of Education of China for Developmental Genes and Human Disease, Department of Genetics and Developmental Biology, Southeast University Medical School, Nanjing, Jiangsu Province, P.R. China.
authors.forename: Lianhong
authors.initials: L
authors.lastname: Xu
authors.forename: Yuqing
authors.initials: Y
authors.lastname: Shen
authors.forename: Mei
authors.initials: M
authors.lastname: Xia
authors.forename: Fengqing
authors.initials: F
authors.lastname: Miao
authors.forename: Chuanlai
authors.initials: C
authors.lastname: Shen
authors.forename: Wei
authors.initials: W
authors.lastname: Xie
authors.forename: Jianqiong
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000071181:ATP Binding Cassette Transporter, Subfamily B, Member 2; D018528:ATP-Binding Cassette Transporters / Q000235:genetics / Q000378:metabolism; D006528:Carcinoma, Hepatocellular / Q000276:immunology* / Q000473:pathology / Q000821:virology; D045744:Cell Line, Tumor; D003602:Cytotoxicity, Immunologic; D006680:HLA Antigens / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D006515:Hepatitis B virus / Q000276:immunology* / Q000472:pathogenicity; D019694:Hepatitis B, Chronic / Q000276:immunology* / Q000473:pathology / Q000821:virology; D006801:Humans; D057131:Immune Evasion; D007694:Killer Cells, Natural / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation
chemical_list: D000071181:ATP Binding Cassette Transporter, Subfamily B, Member 2; D018528:ATP-Binding Cassette Transporters; D006680:HLA Antigens; C073119:TAP1 protein, human