Department of Surgery, University of Pittsburgh, Pittsburgh, PA 15213 USA.
State Key Laboratory of Oral Diseases, Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041 China.
Mil Med Res. 2017 Feb 2;4:3. doi: 10.1186/s40779-017-0115-8. eCollection 2017.
Sepsis remains a major clinical problem with high morbidity and mortality. As new inflammatory mediators are characterized, it is important to understand their roles in sepsis. Interleukin 33 (IL-33) is a recently described member of the IL-1 family that is widely expressed in cells of barrier tissues. Upon tissue damage, IL-33 is released as an alarmin and activates various types of cells of both the innate and adaptive immune system through binding to the ST2/IL-1 receptor accessory protein complex. IL-33 has apparent pleiotropic functions in many disease models, with its actions strongly shaped by the local microenvironment. Recent studies have established a role for the IL-33-ST2 axis in the initiation and perpetuation of inflammation during endotoxemia, but its roles in sepsis appear to be organism and model dependent. In this review, we focus on the recent advances in understanding the role of the IL-33/ST2 axis in sepsis.
脓毒症仍然是一个主要的临床问题，具有很高的发病率和死亡率。随着新的炎症介质的特征被描述出来，了解它们在脓毒症中的作用非常重要。白细胞介素 33（IL-33）是最近描述的 IL-1 家族的一员，广泛表达于屏障组织的细胞中。在组织损伤时，IL-33 作为警报素释放，并通过与 ST2/IL-1 受体辅助蛋白复合物结合，激活固有和适应性免疫系统的各种类型的细胞。IL-33 在许多疾病模型中具有明显的多效性功能，其作用受到局部微环境的强烈影响。最近的研究确立了 IL-33-ST2 轴在内毒素血症期间炎症的启动和持续中的作用，但它在脓毒症中的作用似乎取决于机体和模型。在这篇综述中，我们重点介绍了理解 IL-33/ST2 轴在脓毒症中的作用的最新进展。
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