Figure 6.
Targeting endothelial tPA-dependent NMDAR signaling with Glunomab reduces invasion of the ischemic brain tissues by circulating inflammatory cells. (A) Schematic representation of the experimental protocol. (B) Representative flow cytometry dot plots and gating strategy used for quantification of CD11b+CD45low microglia, CD11b+CD45hi activated microglia or macrophages and CD11b+CD45+Ly6G+ neutrophils, 5 days after stroke in ipsilateral mice brain. (C) Flow cytometry quantification of microglia, activated microglia or macrophages, and neutrophils 5 days after stroke in ipsilateral mice brain in the Ctrl group (n = 6), STZ group (n = 5), STZ-rtPA group (n = 5), STZ-Gluno group (n = 5), and STZ-Gluno-rtPA group (n = 5); ∗P < .05; ordinary 1-way ANOVA; Tukey multiple comparisons. (D) Representative flow cytometry dot plots and gating strategy used for quantification of CD3+ T cells, CD3+CD8+ cytotoxic T cells, and CD3+CD4+ regulatory/helper T cells, 5 days after stroke in ipsilateral mice brain. (E) Flow cytometry quantification of CD3+ T cells, CD3+CD8+ cytotoxic T cells, and CD3+CD4+ regulatory/helper T cells, 5 days after stroke in ipsilateral mice brain in the Ctrl group (n = 6), STZ group (n = 5), STZ-rtPA group (n = 5), STZ-Gluno group (n = 5), and STZ-Gluno-rtPA group (n = 5); ∗P < .05; ordinary 1-way ANOVA; Tukey multiple comparisons.