Figure 5.
Figure 5. rF-TRICOM–infected B cells versus CD40L-activated B cells to stimulate IFN-γ production by antigen-specific T-cell lines. (A) CEA-specific V8T cells (0.5 × 106/mL) were stimulated with irradiated allogeneic B cells isolated from PBMCs that were infected with rF-TRICOM or activated for 24 hours in the presence of 1 μg/mL of CD40L. As control, B cells also were infected with FP-WT. For each condition, APCs were pulsed with 25 μg/mL of CAP1-6D peptide or without peptide. Supernatants were collected after 24 hours of stimulation. (B) MUC-1–specific T cells (0.5 × 106/mL) were stimulated with irradiated allogeneic B cells isolated from PBMCs that were infected with rF-TRICOM or activated for 24 hours in the presence of 1 μg/mL of CD40L. As control, B cells were infected with FP-WT. For each condition, APCs were pulsed with 50 μg/mL of MUC-1 peptide or without peptide. Supernatants were collected after 48 hours of stimulation. Error bars represent SD of multiple determinations.

rF-TRICOM–infected B cells versus CD40L-activated B cells to stimulate IFN-γ production by antigen-specific T-cell lines. (A) CEA-specific V8T cells (0.5 × 106/mL) were stimulated with irradiated allogeneic B cells isolated from PBMCs that were infected with rF-TRICOM or activated for 24 hours in the presence of 1 μg/mL of CD40L. As control, B cells also were infected with FP-WT. For each condition, APCs were pulsed with 25 μg/mL of CAP1-6D peptide or without peptide. Supernatants were collected after 24 hours of stimulation. (B) MUC-1–specific T cells (0.5 × 106/mL) were stimulated with irradiated allogeneic B cells isolated from PBMCs that were infected with rF-TRICOM or activated for 24 hours in the presence of 1 μg/mL of CD40L. As control, B cells were infected with FP-WT. For each condition, APCs were pulsed with 50 μg/mL of MUC-1 peptide or without peptide. Supernatants were collected after 48 hours of stimulation. Error bars represent SD of multiple determinations.

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