From IL-15 to IL-33: the never-ending list of new players in inflammation. Is it time to forget the humble aspirin and move ahead?

The study of the inflammatory response has seen a tremendous expansion over the last 30 years. Advancements in technology and better knowledge of the ethiopathogenesis of several inflammatory conditions have facilitated this process allowing researchers to almost reach the core of problem. Thus, we now know that inflammation can be manifested in many different ways depending on the context that has elicited it. Viral and infectious, allergic and autoimmune, carcinogenic and resolutive are just a few examples of how inflammation can disguise itself. However, and most intriguingly, it appears that the more we try to discover "an ideal target" and delineate borders for a specific class of inflammatory conditions the more we find similarities, overlaps or often links that we did not predict. These somehow disappointing findings have pushed researchers towards a frantic search for new and more "reliable" targets. As result, we have recently seen a surge of many novel mediators of inflammation. If we just limit our focus to inflammatory cytokines, the main topic of this commentary, the list seems never-ending: IL-15, IL-17, IL-18, IL-21, IL-22, IL-23, IL-27 and IL-33. Are these cytokines destined to supersede prostaglandins and other autacoids for their key role in inflammation? Are we going to see a cheap and effective alternative to aspirin on the supermarket shelves in the next few years? Here we summarize the most recent findings on the biological effects of these new inflammatory cytokines and discuss how these discoveries might influence our current view on therapeutic approaches to treat inflammation.