the different immunoregulatory functions of mesenchymal stem cells in patients with low-risk or high-risk myelodysplastic syndromes不同的间充质干细胞的免疫调节功能在低风险或高危骨髓增生异常综合征患者.pdfVIP
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the different immunoregulatory functions of mesenchymal stem cells in patients with low-risk or high-risk myelodysplastic syndromes不同的间充质干细胞的免疫调节功能在低风险或高危骨髓增生异常综合征患者
The Different Immunoregulatory Functions of
Mesenchymal Stem Cells in Patients with Low-Risk or
High-Risk Myelodysplastic Syndromes
1 1 2 2 2 2
Zhigang Zhao *, Zhenling Wang , Qiubai Li , Weiming Li , Yong You , Ping Zou
1 Department of Hematology, The Oncology Hospital of Tianjin Medical University, Tianjin, P.R. China, 2 Department of Hematology, Institute of Hematology, Tongji
Medical College of Huazhong University of Science and Technology, Wuhan, P.R. China
Abstract
Myelodysplastic syndrome (MDS) are a group of progressive, clonal, neoplastic bone marrow disorders characterized by
hematopoietic stem cell dysregulation and abnormalities in the immune system. Mesenchymal stem cells (MSC) have
gained further interests after the demonstration of an immunoregulatory role. Nevertheless, the immunoregulatory function
of MDS bone marrow derived MSC (MDS-MSC) remains poorly defined. In addition, it is not clear whether there are
differences in the regulatory functions between low-risk and high-risk MDS-MSC. In this study, we obtain and expand MSC
from bone marrow of patients with MDS. Our results show that there are significant differences in the immunoregulatory
functions between low-risk and high-risk MDS-MSC. Compare to low-risk MDS-MSC, high-risk MDS-MSC is associated with
the presence of increased TGF-b1, higher apoptosis, higher immunosuppressive rate and a poor ability of hematopoietic
support. In addition, our results find that there are great differences in the CD4+CD25+Foxp3+Tregs inducible rate between
high-risk MDS-MSC and low-risk MDS-MSC. Compared to high-risk MDS-MSC, the inducible rate of CD4+CD25+Foxp3+Tregs
of low-risk MDS-MSC is lower. At last, we find that MDS-MSC derived TGF-b1 is
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