Department of Immunology, Cleveland Clinic, Cleveland, OH 44195, USA.
Immunol Cell Biol. 2010 Mar-Apr;88(3):257-68. doi: 10.1038/icb.2009.113. Epub 2010 Jan 12.
Mucosal epithelium functions not only as a physical barrier, but also as a regulator of innate and adaptive immune responses against foreign substances and microorganisms. In particular, epithelial cells have been directly implicated in Th2 responses, serving as a critical interface between innate immune responses and Th2 immunity. Emerging studies have revealed the cellular and molecular mechanisms by which the epithelium modulates Th2 responses through the production of a group of epithelial-derived Th2-driving cytokines, including interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin. These epithelial-derived Th2-driving cytokines execute a regulatory function of the epithelium on mucosal immunity by promoting Th2 responses and maintaining the balance of host immune homeostasis and defense against various pathogens. Dysregulation of these Th2-driving cytokines can lead to detrimental Th2-dependent inflammatory responses, often manifested in various forms of allergic and inflammatory diseases.
黏膜上皮不仅作为物理屏障发挥作用，还作为调节固有和适应性免疫应答的调控者，抵御外来物质和微生物。特别地，上皮细胞直接参与 Th2 反应，作为固有免疫应答和 Th2 免疫之间的关键界面。新兴研究揭示了上皮细胞通过产生一组上皮衍生的 Th2 驱动细胞因子（包括白细胞介素-25、白细胞介素-33 和胸腺基质淋巴细胞生成素）来调节 Th2 反应的细胞和分子机制。这些上皮衍生的 Th2 驱动细胞因子通过促进 Th2 反应和维持宿主免疫稳态和抵御各种病原体的防御之间的平衡，对黏膜免疫发挥上皮的调节功能。这些 Th2 驱动细胞因子的失调可导致有害的 Th2 依赖性炎症反应，通常表现为各种形式的过敏和炎症性疾病。
