TGF-beta1 gene-modified, immature dendritic cells delay the development of inflammatory bowel disease by inducing CD4(+)Foxp3(+) regulatory T cells

• Published in: Cellular & molecular immunology Vol. 7; no. 1; pp. 35 - 43
• Main Authors: Cai, Zhijian, Zhang, Wei, Li, Min, Yue, Yinpu, Yang, Fei, Yu, Lei, Cao, Xuetao, Wang, Jianli
• Format: Journal Article
• Language: English
• Published: China 01.01.2010
• Subjects: Animals; Cell Differentiation; Cell Movement; Cells, Cultured; Dendritic Cells - cytology; Dendritic Cells - immunology; Female; Forkhead Transcription Factors - immunology; Inflammatory Bowel Diseases - genetics; Inflammatory Bowel Diseases - immunology; Inflammatory Bowel Diseases - pathology; Inflammatory Bowel Diseases - therapy; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; T-Lymphocytes, Regulatory - immunology; Transforming Growth Factor beta1 - biosynthesis; Transforming Growth Factor beta1 - genetics; Transforming Growth Factor beta1 - immunology
• ISSN: 2042-0226
• DOI: 10.1038/cmi.2009.107

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.