Figure 5.
PSGL-1 is critical for the recruitment of acute MS-derived CD8+Tcells. (A) To determine the role of PSGL-1, CD8+ T cells were isolated from 3 patients with acute MS. Control cells received no treatment, but other cells were treated as described in the legend to Figure 4A. Seven venules were analyzed in total. Venular and hemodynamic parameters (mean ± SD) during the experiments were: D = 44.7 ± 10.9 μm; Vm = 1919 ± 749 μm/s; and WSS = 8.6 ± 2.5 dyne/cm2 for control cells. For anti–PSGL-1 mAb-treated cells, they were: D = 44.7 ± 10.9 μm; Vm = 1905 ± 682 μm/s; WSS = 8.6 ± 3.1 dyne/cm2. To determine the role of VCAM-1, CD8+ T cells were isolated from 3 patients with acute MS. Control cells were injected before mAb administration. Initially, mice received 100 μg mAb anti–VCAM-1 intravenously. After 10 minutes we injected the same number of cells as were injected for control. Six venules were examined. Venular and hemodynamic parameters (mean ± SD) during the experiments were: D = 50.8 ± 5.1 μm; Vm = 2017 ± 964 μm/s; WSS = 7.7 ± 3 dyne/cm2 for control cells. After antibody treatment they were: D = 50.8 ± 5.1 μm; Vm = 2256 ± 1022 μm/s; WSS = 8.6 ± 3.1 dyne/cm2. Bars depict rolling and arrest fractions as percentages of control cells that rolled and arrested in the same venule. □ indicates control; ▪, anti–VCAM-1; and ▦, anti–PSGL-1. Data are expressed as the mean ± SEM. Groups were compared with control using the Kruskall-Wallis test followed by Bonferroni correction of P.*P < .01. (B) Velocity histograms were generated as described in the legend to Figure 1B. n indicates number of rolling cells examined; □, control; and ▪, anti–VCAM-1.

PSGL-1 is critical for the recruitment of acute MS-derived CD8+Tcells. (A) To determine the role of PSGL-1, CD8+ T cells were isolated from 3 patients with acute MS. Control cells received no treatment, but other cells were treated as described in the legend to Figure 4A. Seven venules were analyzed in total. Venular and hemodynamic parameters (mean ± SD) during the experiments were: D = 44.7 ± 10.9 μm; Vm = 1919 ± 749 μm/s; and WSS = 8.6 ± 2.5 dyne/cm2 for control cells. For anti–PSGL-1 mAb-treated cells, they were: D = 44.7 ± 10.9 μm; Vm = 1905 ± 682 μm/s; WSS = 8.6 ± 3.1 dyne/cm2. To determine the role of VCAM-1, CD8+ T cells were isolated from 3 patients with acute MS. Control cells were injected before mAb administration. Initially, mice received 100 μg mAb anti–VCAM-1 intravenously. After 10 minutes we injected the same number of cells as were injected for control. Six venules were examined. Venular and hemodynamic parameters (mean ± SD) during the experiments were: D = 50.8 ± 5.1 μm; Vm = 2017 ± 964 μm/s; WSS = 7.7 ± 3 dyne/cm2 for control cells. After antibody treatment they were: D = 50.8 ± 5.1 μm; Vm = 2256 ± 1022 μm/s; WSS = 8.6 ± 3.1 dyne/cm2. Bars depict rolling and arrest fractions as percentages of control cells that rolled and arrested in the same venule. □ indicates control; ▪, anti–VCAM-1; and ▦, anti–PSGL-1. Data are expressed as the mean ± SEM. Groups were compared with control using the Kruskall-Wallis test followed by Bonferroni correction of P.*P < .01. (B) Velocity histograms were generated as described in the legend to Figure 1B. n indicates number of rolling cells examined; □, control; and ▪, anti–VCAM-1.

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