Supporting Figures

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Fig. 6. MM, but not MGUS or donor, sera inhibit NKG2D-dependent NK cell cytotoxicity. Healthy donor PBMCs were incubated in donor, MGUS, or MM sera for 48 h and washed; NK cells were then purified with magnetic bead selection and tested for lytic activity against ⁵¹Cr-labeled K562 targets. The NKG2D-dependent lysis was determined with the addition of mAb 1D11 (anti-NKG2D) or isotype control mAb. The results are representative of two donors. Points were performed in triplicate. The means are shown, with SD <10%.

Fig. 7. sMM is associated with minimal alterations in NKG2D expression and function. (Left) PBMCs from an sMM patient were evaluated for NKG2D expression on CD56⁺ T cells by flow cytometry. (Center) Magnetic bead-purified NK cells from an sMM patient were tested for lytic activity against K562 targets by surface CD107a mobilization. (Right) PBMCs from an sMM patient were evaluated for NKG2D expression on CD8⁺ T cells by flow cytometry.

Fig. 8. Bortezomib induces ATM phosphorylation in U226 cells, but triggers the degradation of ATM in MM1S cells. MM cells were exposed to 10 mM Bortezomib for the indicated times and then lysed. Immunoblotting was performed for anti-phospho-ATM (ser 1981) and total ATM. Then 10 mg/ml aphidicolin, a DNA polymerase inhibitor, was used as a positive control for the activation of the DNA damage response.