Figure 2.
Figure 2. Evaluation of the potential inhibitory effects of anti-CD4 and antitetraspanin mAbs on the IL-16–mediated chemotaxis of HMC-1 cells and hCB-MCs. The IL-16–mediated migrations of HMC-1 cells (A) and hCB-MCs (B) were evaluated in the presence of varied amounts and combinations of anti-CD4, anti-CD9, anti-CD63, and anti-CD81 mAbs. Results (mean ± SD, n = 3) are expressed as a percentage of that obtained for replicate IL-16–treated cells cultured in the absence of a mAb. In each instance, 200 000 cells were added to the upper chamber in the chemotaxis assay. In the absence of a blocking mAb, IL-16 induced the migration of 223 ± 8 HMC-1 cells/3 high-power fields and 44 ± 5 hCB-MCs/3 high-power fields through the membrane in the 3-hour assay. Thus, in this assay, HMC-1 cells are more responsive to IL-16 than hCB-MCs.

Evaluation of the potential inhibitory effects of anti-CD4 and antitetraspanin mAbs on the IL-16–mediated chemotaxis of HMC-1 cells and hCB-MCs. The IL-16–mediated migrations of HMC-1 cells (A) and hCB-MCs (B) were evaluated in the presence of varied amounts and combinations of anti-CD4, anti-CD9, anti-CD63, and anti-CD81 mAbs. Results (mean ± SD, n = 3) are expressed as a percentage of that obtained for replicate IL-16–treated cells cultured in the absence of a mAb. In each instance, 200 000 cells were added to the upper chamber in the chemotaxis assay. In the absence of a blocking mAb, IL-16 induced the migration of 223 ± 8 HMC-1 cells/3 high-power fields and 44 ± 5 hCB-MCs/3 high-power fields through the membrane in the 3-hour assay. Thus, in this assay, HMC-1 cells are more responsive to IL-16 than hCB-MCs.

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