TGF-β1 gene-modified, immature dendritic cells delay the development of inflammatory bowel disease by inducing CD4+Foxp3+ regulatory T cells

被引：32

作者：

Cai, Zhijian ^{[1
]}

Zhang, Wei ^{[1
]}

Li, Min ^{[1
]}

Yue, Yinpu ^{[1
]}

Yang, Fei ^{[1
]}

Yu, Lei ^{[1
]}

Cao, Xuetao ^{[1
,2
,3
]}

Wang, Jianli ^{[1
]}

机构：

[1] Zhejiang Univ, Sch Med, Inst Immunol, Hangzhou 310058, Zhejiang, Peoples R China

[2] Second Mil Med Univ, Inst Immunol, Shanghai, Peoples R China

[3] Second Mil Med Univ, Natl Key Lab Med Immunol, Shanghai, Peoples R China

来源：

CELLULAR & MOLECULAR IMMUNOLOGY | 2010年 / 7卷 / 01期

基金：

中国国家自然科学基金; 国家高技术研究发展计划(863计划);

关键词：

DCs; IBD; TGF-beta; 1; Treg; EXPRESSION; TOLERANCE; IMMUNITY;

D O I：

10.1038/cmi.2009.107

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

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-beta 1 (TGF-beta 1) 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-beta 1-modified bone marrow-derived imDCs may have a therapeutic effect to IBD. Cellular & Molecular Immunology (2010) 7, 35-43; doi:10.1038/cmi.2009.107

引用

页码：35 / 43

页数：9

共 23 条

[1]

Immunomodulatory therapeutic effect of glatiramer acetate on several murine models of inflammatory bowel disease [J].