Fig. 5.
Fig. 5. Inhibitory activity of antagonistic HA-1 peptides on the number of IFN-γ–producing HA-1–specific T cells in the PBMCs of a patient with GvHD. / After SCT, PBMCs were stimulated in triplicate for 72 hours with HA-1− donor EBV-BLCLs pulsed with 0.1 μg/mL peptide. Antagonist peptides were added in the assay. The IFN-γ spots were visualized and counted as indicated in “Materials and methods.” Percentage inhibition of IFN-γ producing T cells was calculated as follows: (1 − (mean frequency of IFN-γ–producing cells in the presence of the antagonist peptide)/(mean frequency of IFN-γ–producing cells in the absence of the antagonist peptide) × 100%. The frequency of IFN-γ–producing HA-1–specific T cells in the absence of the antagonist peptide was 96 per 105 PBMCs.

Inhibitory activity of antagonistic HA-1 peptides on the number of IFN-γ–producing HA-1–specific T cells in the PBMCs of a patient with GvHD.

After SCT, PBMCs were stimulated in triplicate for 72 hours with HA-1 donor EBV-BLCLs pulsed with 0.1 μg/mL peptide. Antagonist peptides were added in the assay. The IFN-γ spots were visualized and counted as indicated in “Materials and methods.” Percentage inhibition of IFN-γ producing T cells was calculated as follows: (1 − (mean frequency of IFN-γ–producing cells in the presence of the antagonist peptide)/(mean frequency of IFN-γ–producing cells in the absence of the antagonist peptide) × 100%. The frequency of IFN-γ–producing HA-1–specific T cells in the absence of the antagonist peptide was 96 per 105 PBMCs.

Close Modal

or Create an Account

Close Modal
Close Modal