肿瘤细胞治疗研究
英文原题：Regulation of CD38 on Multiple Myeloma and NK Cells by Monoclonal Antibodies.
Regulation of CD38 on Multiple Myeloma and NK Cells by Monoclonal Antibodies.
CD38在多发性骨髓瘤（MM）细胞上高表达，并在调控肿瘤发生发展中发挥作用。
CD38在多发性骨髓瘤（MM）细胞上高表达，并在调控肿瘤发生和发展中发挥作用。CD38单克隆抗体（mAbs）已通过多种机制被用作MM治疗的有效疗法，包括补体依赖性细胞毒作用、抗体依赖性细胞介导的细胞毒作用、抗体依赖性细胞吞噬作用、程序性细胞死亡、酶调节和免疫调节。尽管CD38 mAbs抑制MM细胞的增殖和存活，但对抗肿瘤NK细胞有显著副作用。需要进一步评估NK介导的免疫反应，以尽量减少NK细胞丢失的不良影响。应尽量减少CD38 mAbs对CD38高表达NK细胞的杀伤作用，并最大化CD38低/阴性NK细胞与CD38 mAbs的潜在联合，以更好地从其抗MM治疗疗效中获益。CD38 mAb对MM的疗效可通过与免疫调节酰亚胺药物（IMiDs）、蛋白酶体抑制剂（PIs）、抗程序性死亡1（PD-1）/程序性死亡配体1（PD-L1）抗体或细胞疗法的联合治疗来最大化，用于MM的治疗，尤其是在复发或难治性MM（R/R MM）和耐药MM患者中。
CD38 is highly expressed on multiple myeloma (MM) cells and plays a role in regulating tumor generation and development. CD38 monoclonal antibodies (mAbs) have been used as an effective therapy for MM treatment by various mechanisms, including complement-dependent cytotoxic effects, antibody-dependent cell-mediated cytotoxicity, antibody-dependent cellular phagocytosis, programmed cell death, enzymatic modulation, and immunomodulation. Although CD38 mAbs inhibit the proliferation and survival of MM cells, there are substantial side effects on antitumoral NK cells. The NK-mediated immune response needs to be further evaluated to minimize the adverse effects of NK cell loss. The killing effect of CD38 mAbs on CD38 high NK cells should be minimized and the potential combination of CD38 low/- NK cells and CD38 mAbs should be maximized to better benefit from their therapeutic efficacy against MM. CD38 mAb effects against MM can be maximized by combination therapies with immunomodulatory imide drugs (IMiDs), proteasome inhibitors (PIs), anti-programmed death 1 (PD-1)/programmed death ligand 1 (PD-L1) antibodies, or cellular therapies for the treatment of MM, especially in patients with relapsed or refractory MM (R/R MM) and drug-resistant MM.
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