Over the last 15 years, the use of various biological therapies has largely improved the way we manage patients with Inflammatory Bowel Diseases (IBDs). Blockade of cytokine synthesis and/or activity is at the forefront of this new era with the success of inhibitors of tumor necrosis factor (TNF)-α. These therapies are however not effective in all IBD patients and efficacy may wane. Moreover, patients treated with anti-TNF-α antibodies can develop severe side-effects and new immune-mediated diseases. Therefore, a new challenge is to elucidate new inflammatory networks in the IBD tissue and develop novel anti-cytokine compounds, which may act in patients who are resistant to or cannot receive anti-TNF-α therapies. In this article we review the available data supporting the pathogenic role of IL-23 and Th17-related cytokines in IBD, and discuss whether and how compounds that control the activity of these cytokines may enter into the therapeutic armamentarium of IBD.
Keywords: IL-23, Th17, IL-17A, IL-21, IBD, Th17-Cytokines, Inflammatory Bowel Diseases, tumor necrosis factor, anti-TNF- antibodies, Crohn's disease, ulcerative colitis, anti-cytokine therapy, interleukin, CD4 cells, interferon, T cells, IL-12, retinoic acid-related orphan receptor, chemokines, polymorphisms, granulocytes, trinitrobenzenesulfonic acid, TNBS-colitis, SCID mice, Bacteroides fragilis, tumours, Neutralization, ABT-874, monoclonal antibody, homeostasis
Rights & PermissionsPrintExport