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. 2011 Apr 11;108(17):7142–7147. doi: 10.1073/pnas.1016569108

Fig. 1.

Fig. 1.

Anti–ErbB-2 mAb therapy requires NK, CD8α+, and CD8β+ cells. (A) H2N100 tumor cells (5 × 105 cells) were injected s.c. into WT and immunodeficient BALB/c mice, and treated with 100 μg of anti–ErbB-2 mAb (clone 7.16.4) or control Ig (clone MAC4) injected i.p. on days 12, 16, 19, and 23. Immunodeficient mice consisted of mice depleted of NK cells (anti-asialo GM1; **P = 0.0097 vs. 7.16.4 + cIg), CD8α+ cells (mAb 53.6.7; *P = 0.0095 vs. 7.16.4 + cIg), or CD4+ cells (mAb GK1.5). (B) Same as A, except that mice were depleted of CD8α+ (*P = 0.0097 vs. 7.16.4 + cIg) or CD8β+ cells (mAb 53.5.8; **P = 0.0097 vs. 7.16.4 + cIg; * vs. **P = 0.0079). (C) Same as A; mice cured of H2N100 tumors were challenged on the opposite flank with 5 × 105 H2N100, H2N67, or H2N113 cells injected s.c. between 42 and 56 d after primary injection (new day 0 on graph). Mice received either 100 μg control Ig (MAC4) or anti-CD8β+ mAb (53.5.8) i.p. on days −1, 0, 7, 14, and 21. (D) Same as A, except that SCID mice were used (*P = 0.0097 SCID + 7.16.4 vs. WT + 7.16.4). Data are mean ± SE of five mice per group. Statistical analyses were performed at time points indicated in figure using the Mann–Whitney test. Depleting or neutralizing mAbs were injected i.p. on days 11, 12, 19, and 26.