Interleukin (IL)-33 was initially recognized as a constituent of the IL-1 cytokine family in 2005. It exerts pleiotropic effects by regulating immune responses via its binding to the receptor ST2 (IL-33R). The IL-33/ST2 pathway has been linked to several inflammatory disorders. In human and rodents, the broad expression of IL-33 in spinal cord tissues and brain indicates its central nervous system (CNS)-specific functions. Growing evidence supports the protective effects of the IL-33/ST2 pathway in ischemic stroke, along with a better understanding of the underlying mechanisms. IL-33 plays a crucial role in the regulation of the release of inflammatory molecules from glial cells in response to neuropathological lesions. Moreover, IL-33/ST2-mediated neuroprotection following cerebral ischemia may be linked to T cell function, specifically regulatory T cells (Tregs). Soluble ST2 (sST2) acts as a decoy receptor in the IL-33/ST2 axis, blocking IL-33 signaling through the membrane ST2 receptor. sST2 has also been identified as a potential inflammatory biomarker of ischemic stroke. Targeting sST2 specifically to eliminate its inhibition of the protective IL-33/ST2 pathway in ischemic brain tissues is a promising approach for the treatment of ischemic stroke.

中文翻译：

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神经炎症的调节：IL-33/ST2 轴在缺血性中风中的作用和机制的进展。

白介素 (IL)-33 最初于 2005 年被认为是 IL-1 细胞因子家族的组成部分。它通过与受体 ST2 (IL-33R) 结合来调节免疫反应，从而发挥多效性作用。IL-33/ST2 通路与多种炎症性疾病有关。在人类和啮齿类动物中，IL-33 在脊髓组织和大脑中的广泛表达表明其具有中枢神经系统 (CNS) 特异性功能。越来越多的证据支持 IL-33/ST2 通路对缺血性中风的保护作用，以及对潜在机制的更好理解。IL-33 在调节胶质细胞释放炎症分子以响应神经病理病变方面发挥着至关重要的作用。此外，脑缺血后 IL-33/ST2 介导的神经保护可能与 T 细胞功能，特别是调节性 T 细胞 (Treg) 相关。可溶性 ST2 (sST2) 作为 IL-33/ST2 轴中的诱饵受体，通过膜 ST2 受体阻断 IL-33 信号传导。sST2 也被确定为缺血性中风的潜在炎症生物标志物。特异性靶向 sST2 以消除其对缺血性脑组织中保护性 IL-33/ST2 通路的抑制是治疗缺血性中风的一种有前途的方法。