Supplementary Figure 1 from Gene-Modified Human α/β-T Cells Expressing a Chimeric CD16-CD3ζ Receptor as Adoptively Transferable Effector Cells for Anticancer Monoclonal Antibody Therapy

PDF file - 5868K, A. Tumor growth in mice treated with activated NK cells combined with rituximab was serially measured using in vivo bioluminescence assay. Two mice (NK-No.1* and NK-No.2**) were euthanized at different time points on day 14 and day 18, respectively. Thereafter, human NK cells and Raji cells persisting in mouse spleen and femoral bone marrow (BM) were measured by flow cytometry. B. Tumor growth in mice similarly treated with cCD16ζ-T cells and rituximab was assessed by in vivo bioluminescence assay. Experiments in Supplementary Fig. S1A and Fig. S1B were conducted in parallel. For comparison with NK-treated mice, a cCD16ζ-T-No.7# mouse was euthanized on day 14, and cCD16ζ-T cells and Raji cells were measured similarly to those in Supplementary Fig. S1A. C. In mice treated with activated NK cells, on day 14, Raji cells were detectable at 8.0% among BM cells, but not in the spleen, as indicated by the bioluminescence assay in Supplementary Fig. S1A. Along with disease progression in Supplementary Fig. S1A from day 14 to day 18, the number of Raji cells increased from 0% to 7.4% in spleen and from 8.0% to 13.7% in BM, respectively. On the other hand, at these two time points, the relative proportion of NK cells remained constant at 4% in the spleen and 0.4% in the BM, respectively. D. Unlike mice treated with NK cells on day 14, higher numbers of effector cells were detectable (9.9% in spleen and 0.8% in BM, respectively), and no Raji cells were detected in either the spleen or BM in the cCD16ζ-T-No.7 mouse. Taken together, the data indicated that the in vivo tumor suppression mediated by cCD16ζ-T cells exploiting ADCC was superior to that mediated by NK cells.