期刊
MOLECULAR IMMUNOLOGY
卷 131, 期 -, 页码 137-143出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.molimm.2020.12.031
关键词
TNFAIP8L2 (TIPE2); Microarray gene expression; Hepatitis B; Apoptosis; Inflammation
资金
- National Natural Science Foundation of China [81873864, 81171578]
- National Outstanding Youth Science Fund Project of National Natural Science Foundation of China [81525012]
- Key Project of Natural Science Foundation of Shandong Province [2016GSF201017, 2017GSF218031]
- Fundamental Research Funds of Shandong University [2018JC020]
TIPE2 regulates apoptosis of HBV-infected hepatocytes by upregulating expression of pro-apoptotic genes, leading to increased cell death in virus-infected cells.
Tumor necrosis factor-a-induced protein-8 like-2 (TNFAIP8L2, TIPE2), a member of TNFAIP8 family, functions as a regulator in inflammation. Our previous studies showed that TIPE2 can negatively regulate HBV-specific CD8+ T lymphocyte functions. But the effect of TIPE2 on the apoptosis of HBV-infected hepatocytes which is very important for eliminating viruses remains unclear. Using gene expression microarray analysis, we find that TIPE2 deficiency can regulate the expression of apoptotic genes in liver tissues from HBV hydrodynamic injection (HI) mouse model. TIPE2 protein was detected in TUNEL staining positive hepatocytes in HBV-infected C57 mice. Interestingly, the TIPE2 expressed hepatocytes were just the HBV infected cells. Furthermore, TIPE2 upregulates the mRNA levels of FasL, Bim and TNFRsF1b which promote cells death, when TIPE2 was transfected into HepG2 cells in vitro. As a result, TIPE2 overexpression cells showed a higher number of apoptotic cells and increased level of cleavage caspase3 compared to controls. Those results indicate that TIPE2 participates in HBV infection by regulating apoptosis of virus-infected hepatocytes.
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