Relationships between the level of chemokine CXCL13 and the distribution of Tfh subsets in peripheral blood of hepatitis B patients and their clinical significance
10.3760/cma.j.issn.0254-5101.2016.05.006
- VernacularTitle:乙型肝炎患者外周血趋化因子 CXCL13表达水平与 Tfh 细胞亚群分布的相互关系及其临床意义
- Author:
Zhiling GAO
;
Yanhua YU
;
Ying SHI
;
Heli NIU
;
Deguang YANG
- Publication Type:Journal Article
- Keywords:
Hepatitis B virus;
T follicular helper cell;
Chemokine CXCL13
- From:
Chinese Journal of Microbiology and Immunology
2016;36(5):354-358
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the distribution of T follicular helper(Tfh)cell subsets in hepa-titis B patients at different immune stages and to clarify the relationships between the level of CXCL13 and the distribution of Tfh cell subsets. Methods Flow cytometry analysis was performed to detect the distribution of Tfh cells. Enzyme-linked immunosorbent assay(ELISA)was performed to measure the levels of CXCL13 in ser-um samples collected from hepatitis B patients. RT-PCR and Western blot assay were used to analyze the expres-sion of CXCL13 in HepG2 and HepG2. 2. 1. 5 cells. Results The percentages of Tfh1 cells were significantly up-regulated at the immune activation(IA)stage,while those of Tfh2 cells were significantly raised at the im-mune tolerance(IT)stage. The percentages of Tfh17 cells in patients at the stage of IT were similar to those in patients at the stage of IA,but were higher than those in responders with HBsAg seroconversion(RP)or healthy controls(HC). The expression of CXCL13 was positively correlated with the percentage of Tfh2 cells. More over,hepatitis B virus(HBV)enhanced the expression of CXCL13 at both transcriptional and translational lev-els. Conclusion HBV might up-regulate the percentage of Tfh2 cells through promoting the expression of CXCL13,which resulted in the induction of immune tolerance. Elucidating the functions of Tfh1,Tfh2 and Tfh17 cells and understanding the type conversion mechanism among the three subsets are important for further researches on HBV-induced immunosuppression.
