Table 1.
Summary of Inhibition of KIM 127–stimulated THP-1 Adhesion to GP Ibα by Antibodies or Soluble Ligands
| Antibody or ligand | Receptor (epitope) | Percent inhibition |
|---|---|---|
| IB4 | Anti-CD18 | 99 ± 1 |
| TS1/22 | Anti-CD11a (I domain) | 10 ± 13 |
| LPM19c | Anti-CD11b (I domain) | 92 ± 12 |
| Polyclonal | Anti-GP Ibα | 80 ± 17 |
| Polyclonal | Rabbit IgG control | 16 ± 20 |
| VM16d | Anti-GP Ibα (aa residues 201–268) | 83 ± 16 |
| AP1 | Anti-GP Ibα (aa residues 201–268) | 86 ± 10 |
| AK2 | Anti-GP Ibα (aa residues 36–59) | 16 ± 6 |
| SZ2 | Anti-GP Ibα (sulfated tyrosine residues 269–282) | 8 ± 6 |
| WM23 | Anti-GP Ibα (macroglycopeptide) | 11 ± 5 |
| 7E3 | Anti-GP IIb-IIIa, -αvβ3, –Mac-1 | 16 ± 8 |
| 10E5 | Anti-GP IIb-IIIa | 18 ± 6 |
| Fibrinogen (2 μM) | Mac-1 | 99 ± 1 |
| P2γ377–395 (10 μM) | Mac-1 | 0 |
| Heparin (200 U/ml) | Mac-1 | 93 ± 9 |
| vWF A1 (20 μg/ml) | GP Ibα | 83 ± 13 |
The adhesion of cytokine-treated THP-1 cells to glycocalicin (GP Ibα)–coated microtiter wells was stimulated by the addition of KIM 127 (5 μg/ml) in the presence and absence of antibodies directed to or soluble ligands of Mac-1 and GP Ibα. Polyclonal antibodies were added at 20 μg/ml and purified mAbs at 10 μg/ml as described in Materials and Methods. Soluble ligand concentrations are indicated. CD11/CD18 mAbs included IB4, TS1/22, and LPM19c; GP Ibα mAbs used were AK2, AP1, VM16d, SZ2, and WM23. Data are expressed as percent inhibition of maximal KIM-stimulated adhesion by the antibodies or soluble ligands (mean ± SD, n = 3–5). aa, amino acids.