Targeting T cell metabolism and polarization to modulate post-stroke immune responses and improve outcomes
Juliane Gellrich·Antje Vogelgesang·Imke Reich·Johanna Ruhnau·Stefan Groß·Susanne H. Kirsch·Rolf Müller·Juliane Schulze·Nora Bödecker
Background T cells drive post-stroke secondary brain injury, with the Th17/Treg balance shaping post-stroke inflammation. Soraphen A (SorA) inhibits Th17 polarization while preserving Tregs. We examined SorA’s effects on post-stroke T cell activation – distinguishing antigen-specific from bystander activation – including inflammatory conditions induced by LPS. Methods Male Nur77 GFP mice (12–14 weeks) underwent tMCAO. At reperfusion, mice received intraperitoneal LPS or vehicle; SorA or vehicle