Figure 1.

CD8⁺ T cell but not NK1.1⁺-cell depletion reduces infarct size and improves sensorimotor function. A, Representative plots from blood of isotype control (IgG), CD8⁺ cell-depleted (anti-CD8), and NK1.1⁺ cell-depleted (anti-NK1.1) mice. B, FACS analysis of the kinetics of CD8⁺ T-cell and NK1.1⁺-cell depletion in blood and spleen 6 h, 24 h, 3 d, 7 d, and 14 d after antibody injection. CD8⁺ T cells are shown as ratio within the CD3⁺ T cell population. NK cells are shown as percentage of whole leukocytes. Whiskers show the 10th to 90th percentiles. C, Representative cresyl violet-stained coronal sections after pMCAO with cortical infarcts and 30 min tMCAO with striatal lesions from IgG, anti-CD8, and anti-NK1.1 mice. D, Infarct volume of IgG and anti-CD8-treated mice 12 h, 24 h, 3 d, 7 d, and 14 d after pMCAO (on the left) (n = 10 per group, *p < 0.05). Right, Infarct volume of IgG and anti-CD8 mice at 7 d after pMCAO when antibody was injected 5 or 12 h after ischemia induction (n = 9 per group, *p < 0.05). Whiskers show 5th to 95th percentiles. E, Sensorimotor asymmetry of IgG- and anti-CD8-treated mice was assessed as right/left turn ratio in the corner test at the indicated time points after pMCAO (n = 10 per group, *p < 0.05). F, Left, Infarct volume of IgG- and anti-CD8-treated mice 24 h and 7 d after 30 min tMCAO (n = 10 per group, *p < 0.05). Right, Fine motor skills of IgG- and anti-CD8-treated mice were measured in the cylinder test at the indicated time points after tMCAO. Motor asymmetry was assessed as left/all forepaw use and was normalized on performance before tMCAO (n = 12 per group, *p < 0.05). G, Infarct volume of IgG and anti-NK1.1 mice 7 d after pMCAO and 30 min tMCAO (n = 10 per group). Whiskers show the 5th to 95th percentiles. H, Sensorimotor asymmetry of IgG and anti-NK1.1 mice assessed in the corner test at the indicated time points after pMCAO (n = 10 per group). Data of functional tests are expressed as mean ± SD.