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. 2009 Apr 6;119(5):1251–1263. doi: 10.1172/JCI36022

Figure 6. Differential contribution of NKp46 and DNAM-1.

Figure 6

(A) CFSE-labeled RET cells (2 × 105) were injected i.p. into control IgG– and DNAM-1–treated or NK1.1-depleted B6 mice, and the number of residual RET cells were counted 48 hours later. Representative plots of peritoneal lavage CFSE gating are shown. (B) Quantification of residual cells. Data are mean + SEM of 8–10 mice per group and are pooled from 2 experiments. *P < 0.05 compared with control. (C) NK cells were expanded for 5 days in IL-2, sorted into DNAM-1+ and DNAM-1, recultured for 48 hours, and tested for cytotoxicity at the indicated E:T ratio. Results are representative of 2–3 experiments. (D) NK cells from WT or Ncr1–/– mice were expanded, sorted, recultured as described in C, and injected i.p. into Rag2–/–Il2rg–/– mice (2.5 × 105/mouse) immediately after i.p. injection of 5 × 105 CFSE-labeled RET cells. Residual RET cells were counted following lavage 48 hours later. Results are individual mice from 3 independent experiments. The bar represents the mean of 8–9 mice per group. (E and F) RET cells (105) were injected i.v. into control IgG, anti–DNAM-1–treated or anti-NK1.1–depleted WT or Ncr1–/– mice (E). (F) RET cells (2 × 105) were injected i.v. into WT, Ncr1–/–, or NK1.1-depleted WT mice. Lung metastases were counted 14 days later. Results are from individual mice, and the bar represents the mean of 4–5 (E) and 6–11 (F) mice per group. **P < 0.01.