The pathogenesis of inflammatory diseases involves complex interactions among genetic, environmental and immunologic factors, where the immune system plays a crucial role. The initiating factor may be a commonly present environmental antigen, but the defective mucosal immune response can't downregulate the inflammatory process, the resulting in chronic inflammation and tissue damage. The abnormal amplification of the immune system seems more likely to be a secondary and not a primary factor in the disease. IBD patients exhibit abnormalities in epithelial antigen presentation, and in the cellular and humoral immune system. The role of autoimmunity is unclear in IBD. The inflammatory mediator production and balance is also altered in IBD. Crohn's disease is characterised by a Th1 cytokine profile, while ulcerative colitis is characterised rather by a Th2 cytokine profile. Recent advances in the understanding of the pathogenesis of IBD led to major changes in the treatment of the disease. The newer agents target the key mediators involved in the inflammatory process.