The William Harvey Research Institute, Queen Mary University of London, Barts and The London Medical School, Charterhouse Square, London EC1 M 6BQ, UK.
Biochem Pharmacol. 2010 Feb 15;79(4):525-34. doi: 10.1016/j.bcp.2009.09.015.
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.
过去 30 年来，人们对炎症反应的研究有了巨大的扩展。技术的进步和对几种炎症发病机制的更好认识促进了这一过程，使研究人员几乎能够深入问题的核心。因此，我们现在知道，根据引发炎症的背景，炎症可以以许多不同的方式表现出来。病毒和感染性、过敏和自身免疫性、致癌性和消退性只是炎症如何伪装自己的几个例子。然而，最有趣的是，似乎我们越是试图发现“理想的靶点”，并为特定类别的炎症划定界限，我们就越能发现相似之处、重叠之处，甚至经常是我们没有预测到的联系。这些令人失望的发现促使研究人员疯狂地寻找新的、更“可靠”的靶点。因此，我们最近看到了许多新的炎症介质的涌现。如果我们只将注意力局限于炎症细胞因子，即本评论的主要主题，那么这个列表似乎无穷无尽：IL-15、IL-17、IL-18、IL-21、IL-22、IL-23、IL-27 和 IL-33。这些细胞因子是否注定会因其在炎症中的关键作用而取代前列腺素和其他自体活性物质？在未来几年，我们是否会在超市的货架上看到一种廉价且有效的阿司匹林替代品？在这里，我们总结了这些新的炎症细胞因子的最新生物学作用发现，并讨论了这些发现如何影响我们目前对治疗炎症的治疗方法的看法。
