Figure 1
Figure 1. Antitumor reactivity mediated by γ9δ2TCRs. Peripheral blood T cells were virally transduced with indicated wild-type γ9δ2TCRs or CTE-engineered γ9δ2TCRs and tested against Daudi (A,C) in a 51Cr-release assay (E:T, 3:1). Specific lysis is indicated as the fold change 51Cr-release measured in the supernatant after 5 hours compared with reactivity of γ9-G115wt/δ2-G115wt-engineered T cells (B,D) in an IFNγ ELISA in the presence of indicated amounts of pamidronate or (E) different E:T ratios. (F) Percentages of cell-cell conjugates of Daudi and T cells engineered with indicated γ9δ2TCR were determined by flow cytometry. Data represent the means ± SD. *P < .05; **P < .01; and ***P < .001 by 1-way ANOVA.

Antitumor reactivity mediated by γ9δ2TCRs. Peripheral blood T cells were virally transduced with indicated wild-type γ9δ2TCRs or CTE-engineered γ9δ2TCRs and tested against Daudi (A,C) in a 51Cr-release assay (E:T, 3:1). Specific lysis is indicated as the fold change 51Cr-release measured in the supernatant after 5 hours compared with reactivity of γ9-G115wt/δ2-G115wt-engineered T cells (B,D) in an IFNγ ELISA in the presence of indicated amounts of pamidronate or (E) different E:T ratios. (F) Percentages of cell-cell conjugates of Daudi and T cells engineered with indicated γ9δ2TCR were determined by flow cytometry. Data represent the means ± SD. *P < .05; **P < .01; and ***P < .001 by 1-way ANOVA.

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