Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 16, Issue 33, Pages 3656-3660Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/138161210794079164
Keywords
IL-23; Th17; IL-17A; IL-21; IBD
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Funding
- Fondazione Umberto Di Mario (Rome, Italy)
- Giuliani Spa (Milan, Italy)
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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)-alpha. These therapies are however not effective in all IBD patients and efficacy may wane. Moreover, patients treated with anti-TNF-alpha 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-alpha 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.
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