Neuropsychopharmacology Research Group, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario M4N 3M5, Canada.
Neurosci Biobehav Rev. 2013 Mar;37(3):436-47. doi: 10.1016/j.neubiorev.2013.01.021. Epub 2013 Jan 28.
Stroke is a leading cause of physical disability with neurodegenerative sequelae such as dementia and depression causing significant excess morbidity. Stroke severity can be exacerbated by apoptotic cell death in ischemic tissue, of which inflammatory activity is a key determinant. Studies have identified harmful and beneficial sets of T lymphocytes that infiltrate the brain post-stroke and their activation signals, suggesting that they might be targeted for therapeutic benefit. Animal models and human studies implicate interleukin(IL)-17 and its congeners (e.g. IL-23, IL-21) as mediators of tissue damage in the delayed phase of the inflammatory cascade and the involvement of T lymphocytes in propagating IL-17 release. In this review, we highlight the current understanding of IL-17 secreting cells, including sets of CD4(+) αβ and CD4(-) γδ T lymphocytes, as potentially important mediators of brain pathology post-stroke. Interactions between the IL-17 axis and innate pathways, positive feedback mechanisms that prolong or amplify IL-17, and IL-17 regulatory pathways may offer intervention targets to enhance recovery, prevent long-term decline, and improve quality of life.
中风是导致身体残疾的主要原因，其神经退行性后遗症如痴呆和抑郁症导致发病率显著增加。缺血组织中的细胞凋亡可加重中风的严重程度，其中炎症活动是一个关键决定因素。研究已经确定了在中风后浸润大脑的有害和有益的 T 淋巴细胞群及其激活信号，表明它们可能成为治疗的靶点。动物模型和人类研究表明白细胞介素(IL)-17 及其同系物(如 IL-23、IL-21)是炎症级联反应迟发相组织损伤的介质，以及 T 淋巴细胞在传播 IL-17 释放中的作用。在这篇综述中，我们强调了目前对 IL-17 分泌细胞的理解，包括 CD4(+)αβ和 CD4(-)γδ T 淋巴细胞群，它们可能是中风后大脑病理学的重要介质。IL-17 轴与先天途径之间的相互作用、延长或放大 IL-17 的正反馈机制以及 IL-17 调节途径可能为增强恢复、预防长期衰退和提高生活质量提供干预靶点。
