Fig. 6.
Fig. 6. TGF-β decreases CTL-specific lysis against autologous EBV-LCL targets in mock-transduced or nontransduced CTLs but not in HATGF-βRII-Δcyt–transduced CTLs. / Percentage of specific 51Cr release was determined 4 hours after coincubation with autologous LCLs, allogeneic LCLs, and HSB-2 targets. TGF-β was added to CTL cultures 96 hours before cytotoxicity assay. The graphs show the percentage of specific lysis at effector-to-target ratios of 20:1, 10:1, and 5:1 in representative CTL lines generated from a healthy donor (A) and from a patient with Hodgkin disease (B). ▴ indicates CTLs cultured without TGF-β and autologous LCL target; ●, CTLs cultured with TGF-β and autologous LCL target; ░, CTL versus HSB-2 target; ♦, CTLs versus allogeneic (HLA class I mismatch) LCL target.

TGF-β decreases CTL-specific lysis against autologous EBV-LCL targets in mock-transduced or nontransduced CTLs but not in HATGF-βRII-Δcyt–transduced CTLs.

Percentage of specific 51Cr release was determined 4 hours after coincubation with autologous LCLs, allogeneic LCLs, and HSB-2 targets. TGF-β was added to CTL cultures 96 hours before cytotoxicity assay. The graphs show the percentage of specific lysis at effector-to-target ratios of 20:1, 10:1, and 5:1 in representative CTL lines generated from a healthy donor (A) and from a patient with Hodgkin disease (B). ▴ indicates CTLs cultured without TGF-β and autologous LCL target; ●, CTLs cultured with TGF-β and autologous LCL target; ░, CTL versus HSB-2 target; ♦, CTLs versus allogeneic (HLA class I mismatch) LCL target.

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