Fig. 1

Abrogation of IFN-β in mice results in a higher accumulation of CD45^highCD11b⁺ leukocytes within the brain 2 days after tMCAo. a Left panel experimental design: IFN-βKO mice and WT controls underwent tMCAo or sham surgery; behavioral testing was done 24 h, as well as 2 and 7 days after surgery; samples were obtained 2 and 8 days after surgery. Right panel photograph of a TTC-stained brain slice (WT mouse) 24 h after tMCAo reflecting the stereotypical infarct core (white). FLC flow cytometry, IC infarct core, IHC immunohistochemistry, IV infarct volume. b–g Two days post-occlusion, immune and inflammatory cells were extracted from contralateral (Contra) and ipsilateral (Ipsi) brain hemispheres (WT, n = 3 with three brains per n; IFN-βKO mice, n = 3 with three to four brains per n), and different subsets were characterized by flow cytometry analysis. b Representative dot plots showing gates used to discriminate CD11b⁺ cells expressing high or low levels of CD45, as well as respective changes across Contra/Ipsi hemispheres and WT/IFN-βKO animals (as indicated in the figure). Populations: R1 (putative lymphocytes and NK cells), R2 (putative monocytes/macrophages), and R3 (putative granulocytes). FSC forward scatter, SSC side scatter. c Percentage of CD45^highCD11b⁺ cells, (infiltrating) leukocytes, and d CD45^dimCD11b⁺ cells, (brain-resident) microglia. e Micrographs denoting the abundance and typical morphology of CD45⁺ (Cy3, red) cells within the infarct core (striatum) 2 days after tMCAo (WT animal); DAPI counterstain (represented in blue). Scale bars, 50 μm (left panel) and 10 μm (right panel). Number of CD45⁺ cells per mm² in WT and IFN-βKO mice. f–g Percentages of MHCII⁺ (activated) CD45^highCD11b⁺ leukocytes and MHCII⁺ (activated) CD45^dimCD11b⁺ microglia, respectively. *p < 0.05 and **p < 0.01 (Bonferroni correction)