Transplantation of adipose‐derived mesenchymal stem cells into a murine model of passive chronic immune thrombocytopenia

Transfusion - Tập 52 Số 12 - Trang 2551-2558 - 2012
Jianhong Xiao1,2,3, Changran Zhang1,2,3, Yangchun Zhang1,2,3, Xiangzhong Zhang1,2,3, Jiangning Zhao1,2,3, Jiayi Liang1,2,3, Xueyun Zhong1,2,3, Yunxian Chen1,2,3
1From the Department of Hematology, the Department of Internal Medicine, Huang Pu Hospital, and the Department of Joint Surgery, Huangpu Joint Centre, First Affiliated Hospital of Sun Yat-sen University
2the Department of Hematology, Third Affiliated Hospital of Sun Yat-sen University
3the Department of Pathology, Medical College of Ji-nan University, Guangzhou, Guangdong, China.

Tóm tắt

BACKGROUND: Immune thrombocytopenia (ITP) is a bleeding disorder characterized by antibody‐opsonized platelets (PLTs) being prematurely destroyed by macrophages in the reticuloendothelial system. T helper (Th) cells and different Th cytokines play an important role in the pathophysiology of ITP. As immunomodulators, adipose‐derived mesenchymal stem cells (ADSCs) regulate Th cells and show therapeutic effects in autoimmune diseases. However, it is not clear how ADSCs affect ITP. In this study, we explored the specific effects of ADSCs on ITP in mice.STUDY DESIGN AND METHODS: BALB/c mice were randomly divided into three groups: normal controls, ITP controls, and ITP with ADSC transplantation. PLT levels were monitored by an automatic blood cell counter, and the cytokines interferon‐γ (IFN‐γ); interleukin (IL)‐2, ‐4, ‐10, and ‐17; and transforming growth factor‐β1 (TGF‐β1) were analyzed by enzyme‐linked immunosorbent assays.RESULTS: Compared to the untreated ITP mice, the PLT level of the ITP mice significantly increased after ADSC treatment. In the ADSC group, IFN‐γ, IL‐2, and IL‐17 significantly decreased, while IL‐4, IL‐10, and TGF‐β1 increased.CONCLUSION: These findings constitute the first experimental evidence that ADSCs are efficacious in improving PLT levels and reducing the related Th cytokines mediating proinflammatory response in ITP mice, which may provide a scientific basis for using ADSCs as a new therapy for ITP.

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