Fig. 2.
Fig. 2. Ability of TGF-β to inhibit T-cell proliferation is significantly greater in nontransduced CTLs when compared with HATGF-βRII-Δcyt–transduced CTLs. / Nontransduced CTLs, eGFP-transduced CTLs, and HATGF-βRII-Δcyt–transduced CTLs were stimulated with irradiated autologous LCLs and IL-2 ± 5 ng/mL TGF-β1. Proliferative responses were measured after 72 hours of incubation by measurement of3[H] thymidine uptake. The mean percentage of inhibition by TGF-β was measured in nontransduced CTLs (black), eGFP-transduced CTLs (white), and HATGF-βRII-Δcyt–transduced CTLs (gray). The graph represents a pooled analysis of the mean inhibition of TGF-β on3[H] thymidine uptake in the 8 CTL lines tested.

Ability of TGF-β to inhibit T-cell proliferation is significantly greater in nontransduced CTLs when compared with HATGF-βRII-Δcyt–transduced CTLs.

Nontransduced CTLs, eGFP-transduced CTLs, and HATGF-βRII-Δcyt–transduced CTLs were stimulated with irradiated autologous LCLs and IL-2 ± 5 ng/mL TGF-β1. Proliferative responses were measured after 72 hours of incubation by measurement of3[H] thymidine uptake. The mean percentage of inhibition by TGF-β was measured in nontransduced CTLs (black), eGFP-transduced CTLs (white), and HATGF-βRII-Δcyt–transduced CTLs (gray). The graph represents a pooled analysis of the mean inhibition of TGF-β on3[H] thymidine uptake in the 8 CTL lines tested.

Close Modal

or Create an Account

Close Modal
Close Modal