期刊
VIROLOGY
卷 568, 期 -, 页码 31-40出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2022.01.006
关键词
EBV; PD-L1; Lytic reactivation; EBNA2
类别
资金
- Ministry of Education, Culture, Sports, Science and Technology [19K07580, 19K22560, 20H03493]
- Japan Agency for Medical Research and Development [JP20wm0325012, JP21wm0325042]
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [20H03493, 19K22560, 19K07580] Funding Source: KAKEN
Reactivation of EBV leads to increased PD-L1 expression, which is induced through upregulation of EBNA2 and activation of signaling pathways. The expression of PD-L1 varies in different cell types.
Epstein-Barr virus (EBV) is an etiologic agent of infectious mononucleosis and several malignancies. Here, we found that reactivation of EBV resulted in increased programmed cell death-ligand 1 (PD-L1) expression in a cell type-dependent manner. Lytic induction in EBV-positive Akata, AGS, MutuI, and Jijoye cell lines increased PD-L1 levels, but cells such as EBV-negative Akata, MutuIII, and P3HR1 did not have increased PD-L1. EBV in the P3HR1 cell line has a deletion in the EBNA2 gene, while EBV in its parental cell line, Jijoye, has the complete EBNA2 gene. PD-L1 expression by lytic induction was reduced when EBNA2 was knocked down. In addition, pharmacological inhibition indicated involvement of nuclear factor kappa B, mitogen-activated protein kinase, and AKT signaling. These results suggest that EBV likely evades immunity by inducing PD-L1 upon reactivation, through the increased expression of EBNA2 and activation of signaling pathways.
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