VCAM-1 is required for rolling and arrest of acute MS-derived CD4⁺T cells. (A) To determine the role of PSGL-1, CD4⁺ T cells were isolated from 4 patients with acute MS. Control cells received no treatment, whereas other cells were pretreated with 100 μg/mL anti–PSGL-1 mAb for 15 minutes at 25°C in a total volume of 300 μL and were injected through the right carotid catheter. A supplement of up to 100 μg mAb was administered, together with anti–PSGL-1 mAb-treated cells. Ten venules were analyzed. Venular and hemodynamic parameters (mean ± SD) during the experiments were: D = 40.6 ± 10.1 μm; V_m = 1857 ± 410 μm/s; WSS = 8.4 ± 2.2 dyne/cm² for control cells; and D = 40.6 ± 10.1 μm; V_m = 2067 ± 393 μm/s; WSS = 10.2 ± 3.5 dyne/cm² for antibody-treated cells. To determine the role of VCAM-1, CD4⁺ T cells were isolated from 3 patients with acute MS. Control cells were injected before mAb administration. Mice received intravenous administration of 100 μg mAb anti–VCAM-1. After 10 minutes, we injected the same number of cells used for the controls. Six venules were examined. Venular and hemodynamic parameters (mean ± SD) during the experiments were: D = 46.6 ± 21.8 μm; V_m = 2125 ± 448 μm/s; WSS = 10.5 ± 4.6 dyne/cm² for control cells. After antibody treatment, the parameters were: D = 46.6 ± 21.8 μm; V_m = 2743 ± 629 μm/s; WSS = 12.5 ± 5.3 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 mean ± SEM. Groups were compared with control using the Kruskall-Wallis test followed by Bonferroni correction of P.*P < .01; **P < .001. (B) Velocity histograms were generated as described in the legend to Figure 1B. n indicates number of rolling cells examined.