Discerning which mediators drive pathogenesis in chronic inflammatory diseases can be complex: immune cells can release various pathogenic cytokines, and numerous cytokines may either cause one specific disease or many. Human validation and mechanistic studies will be necessary to identify the key immune cells and cytokines for a given inflammatory disorder and to pinpoint which cytokine might be the appropriate target for tackling each disease. In 'Bedside to Bench', Georg Schett et al. discuss how human trials targeting different cytokines suggest the existence of a hierarchical framework of cytokines that defines groups of chronic inflamatory diseases rather differently from the homogenous molecular disease pattern previously assumed. In 'Bench to Bedside', Vijay Kuchroo and Dominique Baeten peruse the role of interleukin-17A as drug target in several autoimmune diseases to highlight how success in the clinic will need understanding of pathogenic pathways and the immunological and tissue context of each inflammatory disease.
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Change history
16 July 2013
In the version of this article initially published, the cell at the intersection of IL-12/23 and ulcerative colitis was light green, when it should have been gray. The cell at the intersection of IL-12/23 and Crohn's disease was gray, when it should have been light green. The errors have been corrected in the HTML and PDF versions of the article
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Schett, G., Elewaut, D., McInnes, I. et al. How Cytokine Networks Fuel Inflammation: Toward a cytokine-based disease taxonomy. Nat Med 19, 822–824 (2013). https://doi.org/10.1038/nm.3260
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DOI: https://doi.org/10.1038/nm.3260
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