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Updated: Jul 10, 2025

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke
Published on: January 3, 2025
Systemic treatment with a selective TNFR2 agonist alters the central and peripheral immune responses and transiently
Estrid Thougaard1, Pernille Vinther Nielsen2, Amalie Forsberg3
1Neurobiology Research, Department of Molecular Medicine, University of Southern Denmark, J. B. Winsløwsvej 21 st, 5000 Odense C, Denmark; BRIDGE - Brain Research - Inter Disciplinary Guided Excellence, Department of Clinical Research, University of Southern Denmark, J.B. Winsløwsvej 19, 5000 Odense C, Denmark.
Abstract:
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.

