FOXP3型
促炎细胞因子
免疫学
免疫系统
流式细胞术
脾细胞
炎症
细胞因子
自身免疫
白细胞介素
医学
免疫性血小板减少症
抗体
作者
Guoyang Zhang,Ping Zhang,Hongyun Liu,Xiaoyan Liu,Shuangfeng Xie,Xiuju Wang,Yudan Wu,Jian-xing Chang,Liping Ma
出处
期刊:Hematology
[Informa]
日期:2017-03-16
卷期号:: 1-8
被引量:9
标识
DOI:10.1080/10245332.2017.1301040
摘要
The improved passive immune thrombocytopenia (ITP) mouse model has been extensively utilized for the study of ITP. However, how closely this model matches the human inflammation state and immune background is unclear. Our study aimed to explore the profile of Th cytokines and Th17/Treg cells in the model.We induced the ITP mouse model by dose-escalation injection of MWReg30. The serum levels of cytokines (IFN-γ, IL-2, IL-4, IL-10, IL-17A, and TGF-β1) were measured by enzyme-linked immunosorbent assay and the frequency of Th17 and Treg cells was measured by flow cytometry. The mRNA expression of Foxp3 and RORrt was measured by real-time PCR.The serum levels of cytokines IFN-γ, TGF-β1, IL-4, and IL-10 were significantly lower in ITP mice. The secretion of serum proinflammatory cytokines IL-2 and IL-17A and the percentage of Th17 cells showed no statistically significant increase. In ITP mice the frequency of Treg cells and mRNA expression of Foxp3 was significantly lower in splenocytes.Our data suggest that the improved passive ITP mouse model does not mimic the autoimmune inflammatory process of human ITP. Compared with human ITP, this model has a similar change in frequency of Treg cells, which may directly or indirectly result from antibody-mediated platelet destruction due to attenuated release of TGF-β.
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