Effect of Different Anti–Class I MoAbs on Binding of MoAb90, Proliferation, and Apoptosis of 3-Day PHA-Activated PBL
| Antibodies . | Specificity* . | Binding Competition† . | % Inhibition of Proliferation‡ . | % Specific Apoptosis‡ . |
|---|---|---|---|---|
| 90 | α1 (A, B, C, G) | 66 | 43.4 ± 5.1 | 38.6 ± 3.5 |
| YTH862 | α1 (A, B, C, G) | 65 | 95.6 ± 3.2 | 51.5 ± 4.6 |
| B9.12.1 | α1 (A, B, C) | 15 | 21.9 ± 4.0 | 9.2 ± 2.5 |
| W6.32 | α2 (A, B, C) | 0 | 4.1 ± 4.3 | 0.9 ± 1.1 |
| TP25.99 | α3 (A, B, C) | 0 | 11.1 ± 3.0 | 10.9 ± 2.7 |
| HC10 | α1/α2 (B) | 0 | 0.7 ± 3.8 | 0.1 ± 0.1 |
| B1.23.2 | ND (B, C) | 0 | 1.3 ± 2.9 | 0.5 ± 2.3 |
| B1.G6 | β2m/α1 | 37 | 21.0 ± 4.5 | 3.0 ± 0.6 |
| BE104 | β2m | 54 | 6.4 ± 1.2 | 0.2 ± 0.7 |
| IgG2a control | ND | 0 | 0.3 ± 2.4 | 0.0 ± 0.0 |
| IgG1 control | ND | 0 | 0.9 ± 2.5 | 0.0 ± 0.0 |
| Antibodies . | Specificity* . | Binding Competition† . | % Inhibition of Proliferation‡ . | % Specific Apoptosis‡ . |
|---|---|---|---|---|
| 90 | α1 (A, B, C, G) | 66 | 43.4 ± 5.1 | 38.6 ± 3.5 |
| YTH862 | α1 (A, B, C, G) | 65 | 95.6 ± 3.2 | 51.5 ± 4.6 |
| B9.12.1 | α1 (A, B, C) | 15 | 21.9 ± 4.0 | 9.2 ± 2.5 |
| W6.32 | α2 (A, B, C) | 0 | 4.1 ± 4.3 | 0.9 ± 1.1 |
| TP25.99 | α3 (A, B, C) | 0 | 11.1 ± 3.0 | 10.9 ± 2.7 |
| HC10 | α1/α2 (B) | 0 | 0.7 ± 3.8 | 0.1 ± 0.1 |
| B1.23.2 | ND (B, C) | 0 | 1.3 ± 2.9 | 0.5 ± 2.3 |
| B1.G6 | β2m/α1 | 37 | 21.0 ± 4.5 | 3.0 ± 0.6 |
| BE104 | β2m | 54 | 6.4 ± 1.2 | 0.2 ± 0.7 |
| IgG2a control | ND | 0 | 0.3 ± 2.4 | 0.0 ± 0.0 |
| IgG1 control | ND | 0 | 0.9 ± 2.5 | 0.0 ± 0.0 |
Abbreviation: ND, not determined.
Specificity represents the different domains of HLA class I molecule or β2m and the class I locus product when determined by immunoprecipitation from mouse-transfected fibroblasts.
Results are expressed as percentage of MFI decrease by addition of biotinylated MoAb90 as described in Materials and Methods.
Cells were cultured during 3 days with PHA (10 μg/mL) and then treated with different MoAbs for 24 hours. Apoptosis was assessed by Hoechst 33342 staining and inhibition of proliferation was determined as the decrease of [3H]TdR incorporation as described in Materials and Methods. Results are expressed as mean ± SD of five independent experiments.