Figure 4
Figure 4. Effects of domain deletion mutations and amino acid substitutions on ICAM-4 binding to CD11c/CD18 transfectants. Adhesion of CD11c/CD18-expressing L cells to plastic-coated native and mutated ICAM-4Fc (0.5 μmg/well). Results are shown as the percentage of CD11c/CD18 transfectant-cell binding relative to native ICAM-4Fc (100%). (A) The binding of CD11c/CD18 transfectants to ICAM-4 domain deletion mutants in the absence or the presence of mAbs 1A1 (anti–ICAM-4) or 3.9 (anti-CD11c). Controls included wells with binding of wild-type L cells and the effect of control antibody (not shown). Background binding of cells to HSA was subtracted. Panel B shows the adhesion of CD11c/CD18 transfectants to a panel of ICAM-4 mutants. The mean ± SD from 3 experiments is shown.

Effects of domain deletion mutations and amino acid substitutions on ICAM-4 binding to CD11c/CD18 transfectants. Adhesion of CD11c/CD18-expressing L cells to plastic-coated native and mutated ICAM-4Fc (0.5 μmg/well). Results are shown as the percentage of CD11c/CD18 transfectant-cell binding relative to native ICAM-4Fc (100%). (A) The binding of CD11c/CD18 transfectants to ICAM-4 domain deletion mutants in the absence or the presence of mAbs 1A1 (anti–ICAM-4) or 3.9 (anti-CD11c). Controls included wells with binding of wild-type L cells and the effect of control antibody (not shown). Background binding of cells to HSA was subtracted. Panel B shows the adhesion of CD11c/CD18 transfectants to a panel of ICAM-4 mutants. The mean ± SD from 3 experiments is shown.

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