%0 Figure %A Selby, Andrew %D 2017 %T The Lancet Gastroenterology & Hepatology Journal Cover July 3rd 2017 %U https://repository.lboro.ac.uk/articles/figure/The_Lancet_Gastroenterology_Hepatology_Journal_Cover_July_3rd_2017/9334538 %2 https://repository.lboro.ac.uk/ndownloader/files/16942514 %K Lancet %K Gastroenterology %K Hepatology %K Studies in the Creative Arts and Writing not elsewhere classified %X Treatment of in ammatory bowel disease at present mainly targets mediators of in ammation to stop or suppress pro-in ammatory processes. Typical examples are steroids, suppression of T cells by thioguanine nucleotides, or antibodies against cytokines such as tumour necrosis factor, interleukin 12, or interleukin 23. In addition to suppression of in ammation, development of therapeutic strategies that support resolution of in ammation or that actively resolve in ammation might be desirable. Resolution of in ammation is now seen as an active process involving speci c mediators (eg, lipid mediators or speci c cytokines) that is mandatory to restore organ function and completely shut down in ammation. The molecular pathways involved in resolution of in ammation have been investigated in recent years and could be adopted in treatment strategies for in ammatory bowel disease. Among these approaches are anti-integrin strategies and means to produce or locally increase restitution or resolution factors, such as restoration of the activity of transforming growth factor-β by anti-SMAD7 antisense oligonucleotides. The potential role of in ammation-resolving lipid mediators (eg, resolvins), however, still warrants further study and clinical development. This Review focuses on the specific role of active resolution of in ammation in in ammatory bowel disease pathophysiology. Potential therapeutic targets based on these pathways are also discussed. %I Loughborough University