The frequency and function of FoxP3~+ regulatory T cell in patients with acute hepatitis B
10.3321/j.issn:1007-8738.2009.11.020
- VernacularTitle:急性乙型肝炎患者FoxP3~+调节性T细胞数量与功能的随访
- Author:
Chenxi QIN
;
Hongwei GAO
;
Ying ZHANG
;
Lei GAO
;
Feng JIA
;
Yonghong ZOU
;
Xiuqing YANG
;
Xueqing GUO
- Publication Type:Journal Article
- Keywords:
hepatitis B;
regulatory T cells;
immunotolerance;
pathogenesis
- From:
Journal of Cellular and Molecular Immunology
2009;25(11):1029-1031
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the dynamic variety of frequency and function of FoxP3~+ regulatory T cells in patients with acute hepatitis B (AHB). METHODS: Peripheral blood mononuclear cells (PBMCs) from 15 AHB patients at acute phase (week 1 of illness), convalescent phase (primary occurrence of both ALT level normalization and HBsAg negative conversion), resolved phase (at least 8 weeks after both ALT normalization and HBsAg seroconversion, and 15 health subjects were analyzed for FoxP3 (Forkhead/winged helix transcription factor) mRNA expression in MACS magnetic beads-purified CD4~+ T cells by real-time RT-PCR assay. The effects of Treg cells on the proliferation of CD4~+CD25~- T cells were examined by a ~3[H]-thymidine incorporation assay. RESULTS: AHB patients presented a significantly higher FoxP3 mRNA expression at convalescent phase than acute phase (t=-6.04, P<0.01) and resolved phase (t=4.45, P<0.01), and healthy controls (t=3.44, P<0.01). We also observed that the suppression efficiency of Treg cells on proliferation of CD4~+CD25~- T cells was lower at acute phase than convalescent phase (t=-5.30, P<0.01) and resolved phase (t=-3.20, P<0.05), but there was no significant difference between healthy controls and any phase of AHB. CONCLUSION: AHB patients presented lower circulating Treg frequency and suppression function at acute phase, and both of them are increased at convalescent phase, and then return to normal level along with disease resolved. This follow-up study furthers our understanding of Treg' s role in immunopathogenesis of hepatitis B.
