Fig. 6.
Fig. 6. F-Ara increases the allogenicity of HMECs for CD8+ CTLs: protective effect of defibrotide. / (A) PBMCs were stimulated with irradiated HMECs in the presence of IL-2 (50 U/mL) for 7 days and were subjected to a 51Cr release assay with untreated (Control) and F-Ara (10 μg/mL)–treated HMECs (24-hour incubation) as target cells. Autolog B-LCL, autologous (effector) Epstein-Barr virus (EBV)–transformed B-lymphoblastoid cells; K 562, target cells for NK cells. Results are given as percentage specific lysis as described in “Materials and methods.” *— : percentage specific lysis of F-Ara–treated HMECs in the presence of anti-MHC class I antibody w6/32. E/T ratio: effector–target ratio. (B) Down-regulation of F-Ara–induced allogenicity of HMECs toward CD8+ CTLs by defibrotide (D). CD8+ PBMCs have been negatively selected (non-CD8+-cell–depleted) by magnetic bead separation. For experimental details, see legend to Figure 6A.

F-Ara increases the allogenicity of HMECs for CD8+ CTLs: protective effect of defibrotide.

(A) PBMCs were stimulated with irradiated HMECs in the presence of IL-2 (50 U/mL) for 7 days and were subjected to a 51Cr release assay with untreated (Control) and F-Ara (10 μg/mL)–treated HMECs (24-hour incubation) as target cells. Autolog B-LCL, autologous (effector) Epstein-Barr virus (EBV)–transformed B-lymphoblastoid cells; K 562, target cells for NK cells. Results are given as percentage specific lysis as described in “Materials and methods.” *— : percentage specific lysis of F-Ara–treated HMECs in the presence of anti-MHC class I antibody w6/32. E/T ratio: effector–target ratio. (B) Down-regulation of F-Ara–induced allogenicity of HMECs toward CD8+ CTLs by defibrotide (D). CD8+ PBMCs have been negatively selected (non-CD8+-cell–depleted) by magnetic bead separation. For experimental details, see legend to Figure 6A.

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