Department of Inflammation Research, Amgen, Seattle, WA 98119, USA.
Clin Exp Allergy. 2010 Feb;40(2):200-8. doi: 10.1111/j.1365-2222.2009.03384.x. Epub 2009 Nov 3.
Besides classic T cell-derived T-helper type 2 (Th2) cytokines such as IL-4, IL-5 and IL-13, tissue-produced cytokines such as thymic stromal lymphopoietin, IL-25 and IL-33 are now recognized as important contributors to allergic inflammation. IL-33 is produced by various tissue dwelling cells and broadly enhances allergic inflammation through its effects on hematopoietic cell types. The environmental or endogenous triggers that provoke IL-33 cellular release may be associated with infection, inflammation or tissue damage. This review summarizes the wide range of documented IL-33 activities on human cellular mediators of inflammation as well as genetic evidence that IL-33 contributes to disease. Finally, there will be a discussion of still unanswered questions regarding the mechanisms by which cytokine activity is generated and IL-33's relationship with other Th2-associated cytokines.
除了经典的 T 细胞衍生的 T 辅助细胞 2（Th2）细胞因子，如 IL-4、IL-5 和 IL-13，组织产生的细胞因子，如胸腺基质淋巴细胞生成素、IL-25 和 IL-33，现在被认为是过敏炎症的重要贡献者。IL-33 由各种组织驻留细胞产生，并通过其对造血细胞类型的影响广泛增强过敏炎症。引发 IL-33 细胞释放的环境或内源性触发因素可能与感染、炎症或组织损伤有关。这篇综述总结了广泛记录的 IL-33 对人类炎症细胞介质的活性，以及 IL-33 对疾病的遗传证据。最后，将讨论有关细胞因子活性产生的机制以及 IL-33 与其他 Th2 相关细胞因子的关系的一些尚未解决的问题。
