Fig. 1.
Fig. 1. Rolling adhesion of L-selectin+ (NALM-6-L) and L-selectin− (NALM-6) cells to activated HCMEC as a function of shear stress. At low shear wall stress (0.6 dyne/cm2 ), NALM-6 cells adhere to TNF-α–activated HCMEC equally well as NALM-6-L cells. At high shear stress (<2.0 dyne/cm2 ), adhesion of NALM-6 cells to activated HCMEC is as low as that of NALM-6-L cells to nonactivated HCMEC. L-selectin dependence to TNF-α–stimulated HCMEC is confirmed by inhibition with anti–L-selectin MoAb LAM1-3 and by a L-selectin-IgG-chimera. MoAb LAM1-12 as a binding control antibody does not reduce NALM-6-L adhesion to activated HCMEC. Mean values ±SEM; *P < .05 versus positive control.

Rolling adhesion of L-selectin+ (NALM-6-L) and L-selectin (NALM-6) cells to activated HCMEC as a function of shear stress. At low shear wall stress (0.6 dyne/cm2 ), NALM-6 cells adhere to TNF-α–activated HCMEC equally well as NALM-6-L cells. At high shear stress (<2.0 dyne/cm2 ), adhesion of NALM-6 cells to activated HCMEC is as low as that of NALM-6-L cells to nonactivated HCMEC. L-selectin dependence to TNF-α–stimulated HCMEC is confirmed by inhibition with anti–L-selectin MoAb LAM1-3 and by a L-selectin-IgG-chimera. MoAb LAM1-12 as a binding control antibody does not reduce NALM-6-L adhesion to activated HCMEC. Mean values ±SEM; *P < .05 versus positive control.

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