The inflammatory bowel diseases (IBD), which include Crohn's disease (CD) and ulcerative colitis (UC), are chronic inflammatory disorders effecting 0.3% of the Western population (Podolsky 2002). CD can affect any part of the gastrointestinal tract, from the oral cavity to the anus, whereas UC is limited to the colon and rectum. The etiology of CD and UC remains unknown, but it probably involves a combination of genetic predisposition, environmental conditions, and abnormalities in immune regulation (Chutkan 2001; Farrell et al. 2001; Podolsky 2002). In particular, the intestinal mucosal immune system has been a major focus of research, as IBD is characterized by a hyper-reactive immune system, underlined by a heavy influx of T cells, B cells, monocytes, and neutrophils into the intestinal mucosa. On the simplest level, an imbalance between pro- and anti-inflammatory mediators leads to chronic inflammation in the gastrointestinal tract of patients with IBD. Specific cytokines important for the induction of mucosal immunity and regulation of the mucosal immune responses include the pro-inflammatory mediators IL-1, IL-6, IL-12 and TNF-a, produced by monocytes and macrophages. In addition, the CD4+ T cells infiltrating the lamina propria (LP) of IBD patients display an altered cytokine profile as compared withhealthyindividuals. LP-derived CD4+ Tcellsfrom CD patients produce increased levels of IFN-y and IL-2, whereas LP-derived CD4+ T cells from UC patients produce increased levels of IL-4 and IL-5 (Farrell et al. 2001). These observations suggest that that the immune responses are Th1 and Th2 screwed in CD and UC patients, respectively.
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