Figure 1.
Figure 1. Mevastatin prevents alkylamine-induced activation and proliferation of Vγ9Vδ2 T cells. (A) PBMCs were cultured for 7 days with 0.5 mM IBA, SBA, or 1 μM ZOL with or without 1 μM mevastatin (MEV), in the presence of rhIL-2, prior to dual staining with anti–Vδ2-FITC and anti–CD3-PerCP antibodies, and then were subjected to FACS analysis of the T cell–gated population. Data shown are from one experiment and representative of 2 further experiments from independent donors. (B) PBMCs were treated with 0.5 mM IBA, IPA, or SBA with or without 1 μM mevastatin, in the presence of rhIL-2, for 48 hours. Conditioned media was harvested and IFN-γ levels measured by enzyme-linked immunosorbent assay (ELISA). Data shown are the mean of experiments with PBMCs from 4 independent donors ± SEM. CTL indicates control.

Mevastatin prevents alkylamine-induced activation and proliferation of Vγ9Vδ2 T cells. (A) PBMCs were cultured for 7 days with 0.5 mM IBA, SBA, or 1 μM ZOL with or without 1 μM mevastatin (MEV), in the presence of rhIL-2, prior to dual staining with anti–Vδ2-FITC and anti–CD3-PerCP antibodies, and then were subjected to FACS analysis of the T cell–gated population. Data shown are from one experiment and representative of 2 further experiments from independent donors. (B) PBMCs were treated with 0.5 mM IBA, IPA, or SBA with or without 1 μM mevastatin, in the presence of rhIL-2, for 48 hours. Conditioned media was harvested and IFN-γ levels measured by enzyme-linked immunosorbent assay (ELISA). Data shown are the mean of experiments with PBMCs from 4 independent donors ± SEM. CTL indicates control.

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