Expression and function of HLA-G in human T-cell leukemia virus type 1-positive T cells
10.3760/cma.j.cn112309-20211122-00396
- VernacularTitle:HLA-G在人T淋巴细胞白血病1型病毒阳性T细胞中的表达及功能
- Author:
Hang DONG
1
;
Lixiang WANG
;
Bo XUE
;
Xiaojia YU
;
Guizeng ZHAO
;
Chenguang ZHANG
Author Information
1. 新乡医学院医学检验学院，新乡 453003
- Keywords:
Human leukocyte antigen G;
Human T-cell leukemia virus type 1;
T lymphocyte;
Infection
- From:
Chinese Journal of Microbiology and Immunology
2022;42(5):376-382
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To analyze the expression of human leukocyte antigen G (HLA-G) in human T-cell leukemia virus type 1 (HTLV-1)-positive T cells, and to investigate its role in the occurrence and development of HTLV-1 infection.Methods:The expression of HLA-G in HTLV-1-positive T cell lines (MT2 and MT4) was detected by Western blot and real-time PCR. HLA-G gene in MT2 and MT4 cells was knocked down by siRNA, and the effects of HLA-G on the expression of HTLV-1 Tax and P19 at mRNA and protein levels were detected by Western blot and real-time PCR. Moreover, the changes in cytokine expression in MT2 and MT4 cells were monitored at RNA level after HLA-G gene silencing. The proliferation ability of MT2 and MT4 cells was analyzed by CCK8. Signal transducer and activator of transcription 3 (STAT3) pathway-related proteins were detected by Western blot.Results:Compared with HTLV-1-negative T cells (Jurkat and MOLT4), the expression of HLA-G increased significantly in MT2 and MT4 cells. After knocking down the HLA-G gene with siRNA in MT2 and MT4 cells, the expression of HTLV-1 Tax and P19 at mRNA and protein levels was decreased, and the expression of antiviral cytokines IFN-γ and TNF-α was increased. The proliferation of MT2 and MT4 cells and STAT3 phosphorylation in these cells were decreased.Conclusions:HTLV-1 could induce T cells to overexpress the immune tolerance molecule HLA-G. Silencing HLA-G gene in HTLV-1-positive T cells could promote the production of antiviral cytokines and reduce IL-6 expression and STAT3 phosphorylation, thereby effectively inhibiting the replication of HTLV-1.
