Crohn's disease (CD) and ulcerative colitis (UC) are the major forms of inflammatory bowel diseases (IBD) in man. They are caused by damage to the lining of the intestine and deeper layers, due to an excessive immune response directed against components of the gut microflora and poorly controlled by counter-regulatory mechanisms. CD and UC are however immunologically distinct. CD-related inflammation is characterized by a marked mucosal infiltration of T lymphocytes secreting T helper type (Th) 1 and Th17 cytokines. In UC, the local immune response is less polarized but may show enhanced production of IL-5, IL-13 and Th17 cytokines. Downstream however CD and UC share important end-stage effector pathways of intestinal injury, mediated by an active cross-talk between immune and non-immune cells. The clarification of the complex networks of immune-inflammatory mediators operating in the gut of IBD patients has led to the identification of new targets that should facilitate the development of novel biological therapies.
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