Inflammatory bowel disease (TBD) is thought to result from inappropriate activation of mucosal immune responses. Recently, further understanding the immunopathophysiology of IBD has provided more specific therapeutic approach such as new drug delivery systems using intestinal microflora, interleukin-7(IL-7)/IL-7R system or inducible-co-stimulator (ICOS) in mucosal T cells as a target for treatment of IBD. Administration of Lactococats lactis secreting interleukin 10 or antibody against ICOS molecule specifically expressed in the mucosal T cells of intestinal inflammation successfully treated the murine colitis. While it has been demonstrated that intesti nal epithelial cells produce IL-7 and that IL-7 serves as a regulatory factor for proliferation of mucosal lymphocytes expressing IL-7R. And intestinal epithelial cell-derived IL-7 plays a crucial role in the organization of mucosal lymphoid tissues and regulating the normal immune response in intestinal mucosa. In a previous study, IL-7 transgenic mice developed chronic colitis, and the essential role of mucosal IL-7/IL-7R-dependent signals was demonstrated in the development of chronic intestinal inflammation. These results indicate that mucosal IL-7/IL-7R-dependent signals are involved in the development of chronic intestinal inflammation in both the mouse model and human disease of the intestinal mucosa. Thus current studies indicate that therapeutic approaches by specific targeting of IL-7R-expressing mucosal T cells may be feasiblein the treatment of human IBD.
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