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Mechanism of dexamethasone-resistant B-cell lymphoma cells escaping cytotoxicity of allogeneic NK cells
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Abstract:
Objective: To observe the change of cytotoxicity of NK cells on dexamethasone-resistant B-cell lymphoma cells, and study its mechanism. Methods: 20 μg/ml dexamethasone (DXM) was added to induce DXM-resistance B lymphoma SU-DHL-4 cells (SU cells). The multidrug resistance of SU cells was named SU-DXM cells. NK cells, sorted by flow cytometry was chosen as an effector, and the cytotoxicity of NK cells on SU and SU/DXM cells was analyzed through flow cytometry at E∶T was 20∶1. Real-time PCR was used to detect the gene expression of MHC class Ⅰ chain-related molecules A/B (MICA/B), UL16 binding protein (ULBP)1, ULBP2 and ULBP3 in both SU and SU/DXM cells. Results: After DXM treatment, the SU/DXM cells were established as a multi-drug-resistant cell line. Compared to SU cells, the cytotoyxicity sensitivity of NK cells on SU/DXM cells was obviously down-regulated (\[3.57±4.22\]% vs \[1138±3.51\]%, P<0.05), and the expressions of NKG2D ligand genes MICA, MICB and ULBP2 were statistically lower in SU/DXM cells (MICA: 0.017±0.006, MICB: 0.682±0.063, and ULBP: 20.773±0.066) than those in SU cells (MICA: 1.014±0.121, MICB: 1.009±0.092, and ULBP2: 0.993±0.108, P<0.05, P<0.01). Conclusion: Devamethasone has the ability to induce SU cells to multi-drug-resistant cells, SU/DXM cells, which resist the cytotoxicity mediated by NK cells, and the low gene expression of NKG2D ligands could be one important cause.
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Project Supported:
Project supported by the Research Program of the Science and Technology Bureau of He’nan Province (No. 0611042000)
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