These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Mechanism of umbilical cord mesenchymal stem cells in the up-regulation of regulatory T cells by transforming growth factor β1 in systemic lupus erythematosus].
    Author: Lu L, Wang DD, Li X, Zeng XF, Sun LY.
    Journal: Zhonghua Yi Xue Za Zhi; 2013 Apr 02; 93(13):980-3. PubMed ID: 23886259.
    Abstract:
    OBJECTIVE: To explore the mechanism of umbilical cord mesenchymal stem cells (UC-MSC) in the up-regulation of peripheral regulatory T cells in patients with systemic lupus erythematosus (SLE). METHODS: Peripheral blood mononuclear cells (PBMC) from 20 SLE patients and normal controls were co-cultured with UC-MSC at different ratios respectively for 72 hours. And the proportions of CD4+CD25+Foxp3+regulatory T cells were analyzed by flow cytometry. PBMC and sera from active SLE patients and normal controls were used to stimulate UC-MSC. The expressions of transforming growth factor β1 (TGF-β1) on UC-MSC were detected by real-time fluorescence quantitative polymerase chain reaction (real-time PCR). The supernatant level of TGF-β1 was determined by enzyme-linked immunosorbent assay (ELISA). And the TGF-β1 small interfering RNA (siRNA) was used to interfere with the TGF-β1 expression on UC-MSC and determine its effect on the regulation of SLE Treg cells. TGF-β1 inhibitor was added into the culture system of UC-MSC and PBMC from active SLE patients to observe its role on the up-regulation of Treg cells by UC-MSC. RESULTS: UC-MSC could dose-dependently up-regulate the peripheral CD4+CD25+Foxp3+Treg proportion in SLE patients. And such an effect was not dependent on cell-cell contact. UC-MSC had no regulatory effect on Treg cells in normal controls. Compared with the non-stimulated and normal PBMC stimulated groups, PBMC from SLE patients significantly promoted TGF-β1 mRNA expression on UC-MSC (relative gene expression was 1.00 ± 0.09, 1.95 ± 0.62, 4.20 ± 2.34 respectively, both P < 0.05). The supernatant level of TGF-β1 was significantly elevated in the presence of SLE PBMC. Sera of SLE patients (5%) enhanced TGF-β1 mRNA expression on UC-MSC and it was significantly higher than fetal bovine serum cultured group (12.19 ± 4.49 vs 1.33 ± 0.06, P < 0.01) and normal individual sera cultured group (2.53 ± 0.72, P < 0.01). Additionally, TGF-β1 siRNA interfered UC-MSC failed to up-regulate Treg cells in SLE patients . Furthermore, TGF-β1 specific inhibitor SB431542 significantly inhibited the regulatory role of UC-MSC on Treg cells in SLE patients. CONCLUSION: Immune microenvironment in SLE patients can significantly stimulate the TGF-β1 expression on UC-MSC and plays an important role in the up-regulation of Treg cells in patients.
    [Abstract] [Full Text] [Related] [New Search]