Figure 6.

NK cell depletion does not abrogate IFN-α/β–dependent rejection of immunogenic sarcomas. (A and B) C57BL/6 WT, Rag2^−/−, and Ifnar1^−/− mice and WT mice treated with either PBS or anti-NK1.1 PK136 mAb were injected s.c. (10⁶ cells/mouse) with 1969 (A) or 7835 (B) unedited MCA sarcoma cells, and growth was monitored over time. Data are presented as mean tumor diameter ± SEM of 4–13 (untreated) or 8 (treated) mice per group from at least two independent experiments. Error bars for Ifnar1^−/− mice reflect progressive growth of 1969 and 7835 tumors in 6/9 mice. (C) WT C57BL/6 mice were treated with either PBS or PK136 mAb, and splenocytes were harvested 2 d later and analyzed by flow cytometry using the NK cell markers DX5 and NKp46. Splenocytes were gated on CD3⁻ cells, and the percentages of DX5⁺NKp46⁺ cells are indicated. Similar results were found when harvested at day 6 (not depicted). (D) WT C57BL/6 mice were treated with PBS or PK136 followed by i.p. injection of 300 µg polyI:C 4 d later. After 24 h, splenocytes were harvested and used as effectors in a standard 4-h cytotoxicity assay with NK-sensitive YAC-1 targets. Specific lysis (in percentage ± SEM) at the indicated effector/target (E:T) ratios is shown for four mice/group assayed in duplicate from two independent experiments. (E) WT C57BL/6 mice were treated with PBS, PK136, or a mixture of anti-CD4 (GK1.5) and anti-CD8 (YTS-169.4) mAbs and injected s.c. with 10⁵ RMA-S cells, and tumor growth was monitored over time. Mean tumor diameter ± SEM for three mice/group is shown, and data are representative of two independent experiments.