The regulatory mechanism of PPAR-γ in TH cell differentiation and its relation with transcription factor T-bet and GATA-3
10.3760/cma.j.issn.0254-5101.2009.01.003
- VernacularTitle:PPAR-γ激动剂吡格列酮对Jurkat T细胞分化的调节作用
- Author:
Fang LIU
;
Wenjuan WANG
;
Chengqiang JIN
;
Hong XIAO
;
Biying ZHENG
;
Qun CHEN
;
Guoming LI
- Publication Type:Journal Article
- Keywords:
PPAR-γ;
TH cell;
T-bet;
GATA-3;
Autoimmune disease
- From:
Chinese Journal of Microbiology and Immunology
2009;29(1):11-15
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of PPAR-γ in the gene expression of T-bet/GATA-3 in Jurkat T cells,and to explore the mechanisms underling this sensitizing effect of the change of TH cell subpopulation group.Methods Jurkat T cells were stimulated with PPAR-γ agonist pioglitazone.TH cell related cytokine IFN-γ and IL-10 was detected by ELISA,and the expression of transcription factors(T-bet and GATA-3)mRNA was detected by RT-PCR.To prove the PPAR-γ-dependent effect.the PPAR-γ-specific antagonist GW9662 was used.Results Stimulated with agonist PPAR-γpioglitazone.the concentration of IFN-γ and IL-10 and the expression of transcription factor T-bet and GATA-3 mRNA were both significantlY decreased in Jurkat T cells obviously,and these actions were dependent on the time and the concentrations of pioglitazone.Added with antagonist GW9662 at the same time,such inhibitory actions of IFN-γ and T-bet expression were recovered.but not IL-10 and GATA-3.Conclusion Pioglitazone can inhibite T cells proliferation and their secretion of cytokines.Pioglitazone can inhibit TH1 cells from secreting cytokines,and it is a PPAR-γ-dependent effect related to T-bet.The inhibition on TH2 is not a PPAR-γ-dependent effect and it is GATA-3 related.
