神经炎症
兴奋剂
医学
冲程(发动机)
肿瘤坏死因子α
炎症
外围设备
免疫系统
全身炎症
刺激
免疫学
受体
内科学
机械工程
工程类
作者
Estrid Thougaard,Pernille Vinther Nielsen,Anton Forsberg,Victoria Phuong,A. Velasco,Agnieszka Włodarczyk,Harald Wajant,Isabell Lang,Jens D. Mikkelsen,Bettina Hjelm Clausen,Roberta Brambilla,Kate Lykke Lambertsen
标识
DOI:10.1016/j.jneuroim.2023.578246
摘要
Ischemic stroke often leaves survivors with permanent disabilities and therapies aimed at limiting detrimental inflammation and improving functional outcome are still needed. Tumor necrosis factor (TNF) levels increase rapidly after ischemic stroke, and while signaling through TNF receptor 1 (TNFR1) is primarily detrimental, TNFR2 signaling mainly has protective functions. We therefore investigated how systemic stimulation of TNFR2 with the TNFR2 agonist NewSTAR2 affects ischemic stroke in mice. We found that NewSTAR2 treatment induced changes in peripheral immune cell numbers and transiently affected microglial numbers and neuroinflammation. However, this was not sufficient to improve long-term functional outcome after stroke in mice.
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