Stroke recovery is limited by chronic inflammation, but how metabolic stress disrupts reparative immunity remains unclear. Here we show that microglial cholesterol 25-hydroxylase (CH25H) promotes white-matter repair by restraining CD8⁺ T-cell activation after ischaemic stroke. Ch25h was suppressed in dietary and genetic models of hypercholesterolaemia and dynamically induced in microglia after stroke. Inducible deletion of Ch25h in CX3CR1-lineage cells impaired survival, neurological and cognitive recovery, enlarged chronic lesions and aggravated myelin loss. Integrated single-cell transcriptomic and cytometric profiling showed that Ch25h-deficient microglia adopted antigen-presenting and T-cell-interacting states, accompanied by expansion and local clustering of activated CD8⁺ T cells. Mechanistically, CH25H loss caused free-cholesterol accumulation and enlarged membrane lipid rafts, increasing MHC-I clustering and antigen presentation. Depletion of CD8⁺ T cells during the repair phase reduced lesion burden, preserved white-matter integrity and rescued survival and cognitive recovery in Ch25h-deficient mice, establishing CD8⁺ T cells as necessary mediators of the phenotype. These findings define a CH25H–cholesterol–lipid raft–MHC-I–CD8 axis that links metabolic dysfunction to failed brain repair and identify microglial cholesterol handling as a therapeutic target for post-stroke recovery.