Daniela De Nitto, Massimiliano Sarra, Maria Laura Cupi, Francesco Pallone and Giovanni Monteleone Pages 3656 - 3660 ( 5 )
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.
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
, , , , Dipartimento di Medicina Interna, Universita Tor Vergata, Via Montpellier, 1, 00133 Rome, Italy.