Related Experiment Video
Updated: Apr 30, 2026

An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices
Published on: February 5, 2015
Th17 cell mediated oligodendrocyte precursor cell arrest drives hippocampal demyelination in diabetic cognitive
Jia-Wei Hu1,2, Hong-Dan Yu1,2, Sheng-Xue Yu1,2
1Department of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, PR China.
None:
Demyelination is pivotal in diabetic cognitive dysfunction, with Th17 cells gaining attention, yet their hippocampal infiltration and mechanisms in diabetes remain unelucidated. Using streptozotocin-induced diabetic mice, we demonstrated Th17 cell infiltration and elevated IL-17A in the hippocampus via CD4/IL-17A immunofluorescence and Western blot. Administering IL-17A neutralizing antibodies (NAbs) improved cognitive performance (Morris water maze: reduced escape latency, increased platform crossings/target quadrant time); attenuated neuroinflammation (reduced IL-17A, TNF-α, IL-1β, and IL-6; increased IL-10 and IL-4; decreased microglial activation/IBA-1); restored blood-brain barrier integrity (increased ZO-1 and occludin); and promoted remyelination (increased MBP and CNPase; decreased NG2 and Olig2; Luxol fast blue). IL-17A NAbs also enhanced phosphorylated ERK1/2. Crucially, co-treatment with the ERK inhibitor PD98059 partially reversed the protective effects of IL-17A NAbs on these parameters. These findings indicate that IL-17A, secreted by infiltrating Th17 cells, exacerbates hippocampal demyelination in DCD by inhibiting oligodendrocyte precursor cell maturation via suppression of the ERK1/2 pathway and concurrently activating microglia to amplify neuroinflammation, ultimately driving cognitive impairment.
More Related Videos
Related Concept Videos
EPS and iPS Cells in Disease Research
Type I Diabetes I: Introduction
Type I Diabetes II: Pathophysiology
Type II Diabetes II: Pathophysiology
Diabetic Neuropathy
Alzheimer Disease ll: Pathophysiology

