Your browser doesn't support javascript.
loading
Rosiglitazone upregulates Foxp3 mRNA expression of CD4+T cells in adults with latent autoimmune diabetes / 中华微生物学和免疫学杂志
Chinese Journal of Microbiology and Immunology ; (12): 264-268, 2008.
Artículo en Chino | WPRIM | ID: wpr-384029
ABSTRACT
Objective To investigate the effect of rosiglitazone on the CD4+regulatory T cells in the patients with latent autoimmune diabetes in adults(LADA).Methods The CIM+T cells from IADA patients were isolated with anti-CD4-dynal magnetic beads.The expression of Foxp3 mRNA,along with peroxisome proliferators activator receptors gamma(PPARγ)mRNA and TGF-131 mRNA was determined.The effect of rosiglitazone on CD4+T cells was measured,after treated with rosiglitazone for 48 h.Cell viability was assessed by Mtit assay.The proliferation was assayed with 3 H-TdR.Two-color staining(anti-CD4,anti-CD25)flow cytometric analysis was employed to measure the percentage of CD4+CD25+T cells of Deriph eral blood.Resuits PPARγmRNA was expressed in peripheral CD4+T lymphocytes.RosiglitazoBe inhibited phytohemagglutinin(PHA)-induced human CD4+T cell proliferation in dose dependence.The percentage of CD4+CD25+T cells showed no significant change after the peripheral blood culture with 1 μmol/Land 10μmot/L rosiglitazone.10 μmol/L of rosiglitazone induced Foxp3 mRNA expression in vitro (3.27fold,P<0.05),whereas TGF-β1 mRNA expression did not change.Furthermore,only 1 μmol/L of rosiglitazone could promote Foxp3 mRNA expression if adding IL-2(10 U/m1)in cultures(3.48 fold.P<O.05).Conclusion Rosiglitazone promotes Foxp3 mRNA expression in CD4+T cells in vivo and in vitro,improving the defective of the regulatory T cells.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Microbiology and Immunology Año: 2008 Tipo del documento: Artículo

Similares

MEDLINE

...
LILACS

LIS

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Microbiology and Immunology Año: 2008 Tipo del documento: Artículo