Fig. 2.
Fig. 2. Engagement of HLA class I α1 domain inhibits DNA synthesis of CD40-activated total, naı̈ve, GC, and memory B cells in response to B-cell growth factors. Tonsil B cells (2 × 104/well) from each subset were cultured on CD32-L cells (5 × 103/well) in the presence of 1 μg/mL anti-CD40 MoAb with either IL-10 (20 ng/mL), IL-4 (50 U/mL), IL-2 (20 U/mL) plus IL-10 or IL-4 plus IL-10, and with control IgG1 or MoAb90 at 1 μg/mL added at the onset of the culture. Proliferation was measured by [3H]TdR incorporation after a pulse with [3H]TdR during the last 16 hours of the culture at the time indicated. Results are expressed as means ± SD of culture triplicates. [3H]TdR uptake of CD32-L cells was less than 500 cpm in the different experiments. This figure is representative of three independent experiments.

Engagement of HLA class I α1 domain inhibits DNA synthesis of CD40-activated total, naı̈ve, GC, and memory B cells in response to B-cell growth factors. Tonsil B cells (2 × 104/well) from each subset were cultured on CD32-L cells (5 × 103/well) in the presence of 1 μg/mL anti-CD40 MoAb with either IL-10 (20 ng/mL), IL-4 (50 U/mL), IL-2 (20 U/mL) plus IL-10 or IL-4 plus IL-10, and with control IgG1 or MoAb90 at 1 μg/mL added at the onset of the culture. Proliferation was measured by [3H]TdR incorporation after a pulse with [3H]TdR during the last 16 hours of the culture at the time indicated. Results are expressed as means ± SD of culture triplicates. [3H]TdR uptake of CD32-L cells was less than 500 cpm in the different experiments. This figure is representative of three independent experiments.

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