Figure 3
Figure 3. Provision of exogenous HLA-C binding peptides rescues expression of HLA-C during bortezomib treatment and also prevents the bortezomib–mediated increase in NK cell–mediated lysis. (A) JJN3 cells were cocultured in the presence or absence of the HLA-C binding peptides during 16 hours treatment with bortezomib. Human β2M was added in the medium. Cells were gated on PI–negative cell population and analyzed by flow cytometry for HLA-C expression. The percentage HLA-C expression was shown. Data were reported as means (± SD) of 3 individual experiments. (B) JJN3 cells were treated with 50 nM bortezomib for 18 hours in the presence or absence of the HLA-C binding peptides or irrelevant peptides. Treated and untreated cells were then used as targets in a standard 4-hour 51Cr release assay. K562 was used as a positive control for maximum lysis. Data were reported as means (± SD).

Provision of exogenous HLA-C binding peptides rescues expression of HLA-C during bortezomib treatment and also prevents the bortezomib–mediated increase in NK cell–mediated lysis. (A) JJN3 cells were cocultured in the presence or absence of the HLA-C binding peptides during 16 hours treatment with bortezomib. Human β2M was added in the medium. Cells were gated on PI–negative cell population and analyzed by flow cytometry for HLA-C expression. The percentage HLA-C expression was shown. Data were reported as means (± SD) of 3 individual experiments. (B) JJN3 cells were treated with 50 nM bortezomib for 18 hours in the presence or absence of the HLA-C binding peptides or irrelevant peptides. Treated and untreated cells were then used as targets in a standard 4-hour 51Cr release assay. K562 was used as a positive control for maximum lysis. Data were reported as means (± SD).

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