Department of Neurology, University Clinics Würzburg, Würzburg, Germany.
1] Department of Neurology, University Clinics Würzburg, Würzburg, Germany [2] Institute of Clinical Epidemiology and Biometry, Comprehensive Heart Failure Center, University of Würzburg, Würzburg, Germany.
J Cereb Blood Flow Metab. 2015 Jan;35(1):6-10. doi: 10.1038/jcbfm.2014.175. Epub 2014 Oct 15.
While the detrimental role of non-regulatory T cells in ischemic stroke is meanwhile unequivocally recognized, there are controversies about the properties of regulatory T cells (Treg). The aim of this study was to elucidate the role of Treg by applying superagonistic anti-CD28 antibody expansion of Treg. Stroke outcome, thrombus formation, and brain-infiltrating cells were determined on day 1 after transient middle cerebral artery occlusion. Antibody-mediated expansion of Treg enhanced stroke size and worsened functional outcome. Mechanistically, Treg increased thrombus formation in the cerebral microvasculature. These findings confirm that Treg promote thrombo-inflammatory lesion growth during the acute stage of ischemic stroke.
虽然非调节性 T 细胞在缺血性中风中的有害作用已得到明确证实,但关于调节性 T 细胞(Treg)的特性仍存在争议。本研究旨在通过应用超激动性抗 CD28 抗体扩增 Treg 来阐明 Treg 的作用。在短暂性大脑中动脉闭塞后第 1 天测定中风结果、血栓形成和脑浸润细胞。抗体介导的 Treg 扩增增强了中风的严重程度并使功能结果恶化。从机制上讲,Treg 增加了大脑微血管中的血栓形成。这些发现证实,Treg 在缺血性中风的急性期促进血栓炎症性病变的生长。