摘要
目的:我们以前报道,msc抑制实验性自身免疫性葡萄膜炎(淡)在动物模型中诱导uveitogenic抗原或抗原T细胞。在这项研究中,我们探讨msc的抑制机制在淡的树突状细胞(dc)。 方法:我们收集了DCs的淋巴结MSC治疗或未经处理的水老鼠,以及骨髓衍生DCs培养体外有或没有MSC治疗。costimulatory CD80分子的水平、CD86 CD40、OX40L和抑制细胞因子的信号(SOCS2,SOCS1和SOCS3)在这些DCs通过流式细胞术分析。CCR-7的表达和MMP-9被实时PCR和西方印迹检查。总蛋白质STAT1和STAT6信号分子及其磷酸化被西方的屁股了。ShRNA STAT1和STAT6分别用来探索STAT1和STAT6击倒DCs的影响。 结果:MSC治疗理气表达CD80、CD86,CD40、OX40L,以及CCR-7 MMP-9,但SOCS1的水平增加,soc 2,SOCS3 DCs。STAT1磷酸化而减少STAT6磷酸化增强在MSC DCs治疗。此外,MSC治疗和STAT1 shRNA同样减少CCR-7和DCs MMP-9水平,抑制R16-specific T细胞的增殖。相比之下,击倒DCs的STAT6 STAT6 shRNA CD80和CD86的表达增加,加速R16-specific T细胞的增殖。 结论:msc抑制DC成熟调节Stat1和Stat6磷酸化淡。
关键词: 实验性自身免疫性葡萄膜炎
Current Molecular Medicine
Title:Mesenchymal Stem Cells Inhibited Dendritic Cells Via the Regulation of STAT1 and STAT6 Phosphorylation in Experimental Autoimmune Uveitis
Volume: 17 Issue: 7
关键词: 实验性自身免疫性葡萄膜炎
摘要: Purpose: We have previously reported that MSCs inhibited experimental autoimmune uveitis (EAU) in rodent models induced by either uveitogenic antigens or antigen-specific T cells. In this study, we explored the inhibitory mechanisms of MSCs on dendritic cells (DCs) in EAU.
Methods: We collected the DCs from the lymph nodes of MSC treated or untreated EAU rats, as well as bone marrow derived DCs cultured in vitro with or without MSC treatment. The levels of costimulatory molecules of CD80, CD86, CD40, OX40L and suppressors of cytokine signaling (SOCS1, SOCS2, and SOCS3) on these DCs were analyzed by flow Cytometry. The expression of CCR-7 and MMP-9 was examined by real time PCR and western blots. Total proteins of STAT1 and STAT6 signaling molecules and their phosphorylation were examined by western blots. ShRNA of STAT1 and STAT6 were respectively employed to explore the influence of STAT1 and STAT6 knockdown on DCs.
Results: MSC treatment down-regulated the expression of CD80, CD86, CD40, and OX40L, as well as CCR-7 and MMP-9, but increased the levels of SOCS1, SOCS 2, and SOCS3 on DCs. STAT1 phosphorylation was reduced while STAT6 phosphorylation was enhanced in MSC treated DCs. Moreover, MSC treatment and STAT1 shRNA equally reduced CCR-7 and MMP-9 levels in DCs, and inhibited the proliferation of R16-specific T cells. In contrast, knockdown of STAT6 in DCs by STAT6 shRNA increased the expression of CD80 and CD86 and accelerated the proliferation of R16-specific T cells.
Conclusion: MSCs inhibit DC maturation by regulating Stat1 and Stat6 phosphorylation in EAU.
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Cite this article as:
Mesenchymal Stem Cells Inhibited Dendritic Cells Via the Regulation of STAT1 and STAT6 Phosphorylation in Experimental Autoimmune Uveitis, Current Molecular Medicine 2017; 17 (7) . https://dx.doi.org/10.2174/1566524018666180207155614
DOI https://dx.doi.org/10.2174/1566524018666180207155614 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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