Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.
Our understanding of the mechanisms and pathways involved in human inflammatory bowel disease (IBD) has grown exponentially in recent decades, leading to the identification of a seemingly never-ending list of potential ‘drugable’ targets. We have learned from the past, however, that all that glitters is not gold and we should exercise some caution when translating results from the bench to the bedside. The most recent example of a promising target gone wrong in IBD concerns IL-17.1
We tend to assume that molecules that are up-regulated during inflammation should constitute potential targets to block. While this may seem logical at first, a more in depth understanding of the mechanisms at play reveals that: (1) during inflammation many regulated genes actually exert protective, regenerative or anti-inflammatory actions; (2) a proportion of those inflammation-dependent genes remain altered even during remission in IBD patients.2 Therefore, in addition to its over-expression, obtaining evidence of the in vivo function of a given pathway is essential before considering the development of a blocking strategy for therapeutic purposes. Unfortunately, the effects of blocking cytokines in vivo have proven highly unpredictable. Cytokines are small proteins well known for their multiple cellular sources, pleiotropic nature and highly context-dependent behaviour, making the consequences of their blockage …
Contributors AS researched, designed and wrote the commentary.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.