TGF-β1 基因修饰的未成熟树突状细胞通过诱导 CD4(+)Foxp3(+)调节性 T 细胞延迟炎症性肠病的发展。
TGF-beta1 gene-modified, immature dendritic cells delay the development of inflammatory bowel disease by inducing CD4(+)Foxp3(+) regulatory T cells.
机构信息
Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
出版信息
Cell Mol Immunol. 2010 Jan;7(1):35-43. doi: 10.1038/cmi.2009.107.
Abstract
Inflammatory bowel disease (IBD) is caused by an uncontrolled immune response in the intestinal lumen, leading to inflammation in genetically predisposed individuals. Immunotherapy may be a promising approach to the treatment of IBD. Here, we show that transforming growth factor-beta1 (TGF-beta1) gene-modified immature dendritic cells (imDCs) could enhance the inhibitory function of imDCs and delay the progress of IBD induced by dextran sodium sulfate in mice. The results of fluorescence-activated cell sorter (FACS) demonstrated that this protective effect is mediated partially by inducing CD4(+)Foxp3(+) regulatory T cells (Tregs) in mesentery lymph nodes to control inflammation. In vitro experiments also supported this hypothesis. In conclusion, we provide evidence that TGF-beta1-modified bone marrow-derived imDCs may have a therapeutic effect to IBD.
摘要
炎症性肠病（IBD）是由肠道腔中免疫反应失控引起的，导致遗传易感性个体发生炎症。免疫疗法可能是治疗 IBD 的一种有前途的方法。在这里，我们表明转化生长因子-β1（TGF-β1）基因修饰的未成熟树突状细胞（imDCs）可以增强 imDC 的抑制功能，并延缓葡聚糖硫酸钠诱导的小鼠 IBD 的进展。荧光激活细胞分选（FACS）的结果表明，这种保护作用部分是通过诱导肠系膜淋巴结中的 CD4 + Foxp3 + 调节性 T 细胞（Tregs）来控制炎症来介导的。体外实验也支持这一假设。总之，我们提供的证据表明，TGF-β1 修饰的骨髓来源的 imDCs 可能对 IBD 具有治疗作用。
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