Figure 6.
Figure 6. Effects of coadministration of chNKG2D-modified T cells with RMA/Rae-1β tumor cells on in vivo tumor growth and generation of host antitumor immunity. (A) chNKG2D (♦)– or vector-only (⋄)–transduced T cells were mixed with RMA/Rae-1β tumor cells at a ratio of 10:1 and injected subcutaneously into the right flank of recipient mice. RMA/Rae-1β cells alone (▴) were also injected as control. The error bars represent SEM. chNKG2D-bearing T cells significantly (P < .05 at days 5-15) suppressed the RMA/Rae-1β tumor growth compared with vector-transduced T cells or tumor alone. (B) Tumor-free mice (•) in the chNKG2D-treated group (A) and age-matched naive mice (○) were challenged with wild-type RMA cells (104) injected subcutaneously into the left flank. A summary of 3 independent experiments is shown. (C) The day before RMA/Rae-1β tumor implantation (day-1), 107 chNKG2D (▪)– or vector-only (□)–transduced T cells were adoptively transferred to mice intravenously. At day 0, tumor cells (105) were implanted subcutaneously at the right flank. The tumor areas are represented as means ± SEM. P < .05 at days 9 to 17. (D) chNKG2D (▴)– or vector-only(▵)–transduced T cells were mixed with wild-type RMA tumor cells at a ratio of 10:1 and injected subcutaneously into B6 mice. RMA cells alone (×) were also injected as control. The error bars represent SEM. There was no significant suppression of RMA tumor growth (P > .05) by chNKG2D-transduced T cells compared with vector-transduced T cells or tumor alone.

Effects of coadministration of chNKG2D-modified T cells with RMA/Rae-1β tumor cells on in vivo tumor growth and generation of host antitumor immunity. (A) chNKG2D (♦)– or vector-only (⋄)–transduced T cells were mixed with RMA/Rae-1β tumor cells at a ratio of 10:1 and injected subcutaneously into the right flank of recipient mice. RMA/Rae-1β cells alone (▴) were also injected as control. The error bars represent SEM. chNKG2D-bearing T cells significantly (P < .05 at days 5-15) suppressed the RMA/Rae-1β tumor growth compared with vector-transduced T cells or tumor alone. (B) Tumor-free mice (•) in the chNKG2D-treated group (A) and age-matched naive mice (○) were challenged with wild-type RMA cells (104) injected subcutaneously into the left flank. A summary of 3 independent experiments is shown. (C) The day before RMA/Rae-1β tumor implantation (day-1), 107 chNKG2D (▪)– or vector-only (□)–transduced T cells were adoptively transferred to mice intravenously. At day 0, tumor cells (105) were implanted subcutaneously at the right flank. The tumor areas are represented as means ± SEM. P < .05 at days 9 to 17. (D) chNKG2D (▴)– or vector-only(▵)–transduced T cells were mixed with wild-type RMA tumor cells at a ratio of 10:1 and injected subcutaneously into B6 mice. RMA cells alone (×) were also injected as control. The error bars represent SEM. There was no significant suppression of RMA tumor growth (P > .05) by chNKG2D-transduced T cells compared with vector-transduced T cells or tumor alone.

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