International Immunopharmacology, Год журнала: 2025, Номер 157, С. 114742 - 114742
Опубликована: Май 3, 2025
Язык: Английский
International Immunopharmacology, Год журнала: 2025, Номер 157, С. 114742 - 114742
Опубликована: Май 3, 2025
Язык: Английский
Neuroscience, Год журнала: 2025, Номер unknown
Опубликована: Апрель 1, 2025
Язык: Английский
Процитировано
0Journal of Neuroinflammation, Год журнала: 2025, Номер 22(1)
Опубликована: Апрель 24, 2025
Microglia and Th17 cells are the major immunopathogenic in multiple sclerosis its animal model of immune aspects, experimental autoimmune encephalomyelitis (EAE). While studies have highlighted distinct roles microglia EAE, it remains unclear whether microglia, as potential professional antigen-presenting cells, activate stabilize effector program EAE-pathogenic vivo; if so, could turn reinforce active state microglia. Our data demonstrate an array mouse models, including active/passive-EAE transgenic mice, a microglia-Th17 feed-forward activation loop drives EAE disease progression through mechanism dependent on both MHC-II, proinflammatory cytokines, inflammatory chemokines well STING→NF-κB pathway cytokines produced by pathogenic cells. We also captured identified molecular properties loop, which two-cell entities microglia-Th17, proved them functional units antigen presentation bi-directional between two cell types. Moreover, ACT001, orphan drug to treat glioblastoma, disrupts this inhibiting thereby alleviating EAE. These findings emphasize importance interactions activations neuroinflammation, provide rationale for further investigation ACT001 therapeutic option diseases driven similar mechanisms.
Язык: Английский
Процитировано
0Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0Current Opinion in Physiology, Год журнала: 2025, Номер unknown, С. 100830 - 100830
Опубликована: Май 1, 2025
Язык: Английский
Процитировано
0International Immunopharmacology, Год журнала: 2025, Номер 157, С. 114742 - 114742
Опубликована: Май 3, 2025
Язык: Английский
Процитировано
0