Fig. 4.
Fig. 4. VLA-4–induced adhesion is mediated by β2integrins LFA-1 and Mac-1. / Myelomonocytic HL60 cells were pretreated with medium (control, not shown), soluble VCAM-1–Fc (40 μg/mL, open bars), or mAb K20 (20 μg/mL, filled bars) for 60 minutes at 37°C. After washing, adhesion to endothelial cell monolayers was performed in the presence or absence of blocking mAbs anti-α4 (mAb HP2.1, 50 μg/mL), anti-αM (mAb CBRM1/5, 50 μg/mL), anti-αL (mAb L15, 20 μg/mL), or anti-β2 integrin (mAb 60.3, 20 μg/mL). Values (mean ± SEM) are displayed as percentage of control adhesion and represent the mean of at least 3 independent experiments. *Indicates P < .01 compared with the respective control (no mAb).

VLA-4–induced adhesion is mediated by β2integrins LFA-1 and Mac-1.

Myelomonocytic HL60 cells were pretreated with medium (control, not shown), soluble VCAM-1–Fc (40 μg/mL, open bars), or mAb K20 (20 μg/mL, filled bars) for 60 minutes at 37°C. After washing, adhesion to endothelial cell monolayers was performed in the presence or absence of blocking mAbs anti-α4 (mAb HP2.1, 50 μg/mL), anti-αM (mAb CBRM1/5, 50 μg/mL), anti-αL (mAb L15, 20 μg/mL), or anti-β2 integrin (mAb 60.3, 20 μg/mL). Values (mean ± SEM) are displayed as percentage of control adhesion and represent the mean of at least 3 independent experiments. *Indicates P < .01 compared with the respective control (no mAb).

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