Fig. 5.
Fig. 5. HATGF-βRII-Δcyt–transduced CTLs sorted for the HA epitope demonstrate a significant resistance to the inhibitory effects of TGF-β on secretion of GM-GSF and IFN-γ when compared with nontransduced CTLs. / EBV-specific CTLs were transduced with the mutant TGF-βRII receptor and then positively selected for the HA tag by flow cytometry by using an anti-HA antibody. TGF-βRII-Δcyt–transduced/sorted CTLs and mock-transduced CTLs were stimulated with irradiated autologous LCLs and IL-2 ± 5 ng/mL TGF-β1. Supernatant removed after 24 hours was analyzed for GM-CSF (A) and IFN-γ (B). The graphs represent a pooled analysis of the mean percentage of inhibition of TGF-β on IFN-γ and GM-CSF release in 8 nontransduced (black) and 3 eGFP-transduced CTL (white) lines versus the 3 HATGF-βRII-Δcyt–transduced CTL (gray) lines sorted for the HA-epitope.

HATGF-βRII-Δcyt–transduced CTLs sorted for the HA epitope demonstrate a significant resistance to the inhibitory effects of TGF-β on secretion of GM-GSF and IFN-γ when compared with nontransduced CTLs.

EBV-specific CTLs were transduced with the mutant TGF-βRII receptor and then positively selected for the HA tag by flow cytometry by using an anti-HA antibody. TGF-βRII-Δcyt–transduced/sorted CTLs and mock-transduced CTLs were stimulated with irradiated autologous LCLs and IL-2 ± 5 ng/mL TGF-β1. Supernatant removed after 24 hours was analyzed for GM-CSF (A) and IFN-γ (B). The graphs represent a pooled analysis of the mean percentage of inhibition of TGF-β on IFN-γ and GM-CSF release in 8 nontransduced (black) and 3 eGFP-transduced CTL (white) lines versus the 3 HATGF-βRII-Δcyt–transduced CTL (gray) lines sorted for the HA-epitope.

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