Using a mouse model, Benakis et al. describe a gut−brain axis of ischaemic stroke, in which the commensal gut microbiota confers a neuroprotective effect by modulating immune cells in the small intestine: bacterial priming of dendritic cells results in an expansion of regulatory T cells, which secrete interleukin-10 (IL-10) to suppress the differentiation of γδ T cells into IL-17+γδ T cells. Although this modulation of immune cells by the microbiota occurs in the gut, its effects are relayed to the brain, owing to the migration of IL-17+γδ T cells from the gut to the meninges following ischaemic stroke, which upregulates cytokine genes that contribute to brain injury through the promotion of neutrophil infiltration. Dysbiosis of the microbiota induced by antibiotic treatment or faecal transplant resulted in an imbalance in this gut−brain axis that was responsible for a more than two-fold increase in the volume of necrotic tissue.