Shimadoi Shigeru, Takami Akiyoshi, Kondo Yukio, Okumura Hirokazu, Nakao Shinji
Department of Cellular Transplantation Biology, Kanazawa University Graduate School of Medicine, 13-1 Takaramachi, Kanazawa, Ishikawa 920-8641, Japan.
Cancer Sci. 2007 Sep;98(9):1368-72. doi: 10.1111/j.1349-7006.2007.00544.x. Epub 2007 Jul 19.
Recent studies suggest that monocytes are the dominant effectors by which rituximab induces cell death in B-cell lymphoma. Because macrophage colony-stimulating factor (M-CSF) can enhance the cytotoxicity of monocytes, the authors examined whether this growth factor can enhance their ability to kill lymphoma cells in vitro. Monocytes derived from a healthy volunteer were cultured for 48 h in the presence or absence of M-CSF. Monocytes stimul ated with M-CSF were significantly more cytotoxic to Daudi B-cell lymphomas than unstimulated monocytes. Flow cytometry revealed that M-CSF increased monocyte expression of Fcgamma receptors III and I by 1.6- and 1.5-fold, whereas the expression of Fcgamma receptor II remained unchanged. These results suggest that pretreatment with M-CSF can improve the therapeutic efficacy of rituximab against intractable CD20(+) lymphoma.
近期研究表明,单核细胞是利妥昔单抗诱导B细胞淋巴瘤细胞死亡的主要效应细胞。由于巨噬细胞集落刺激因子(M-CSF)可增强单核细胞的细胞毒性,作者研究了这种生长因子是否能在体外增强其杀伤淋巴瘤细胞的能力。从一名健康志愿者获取的单核细胞在有或无M-CSF的情况下培养48小时。与未受刺激的单核细胞相比,受M-CSF刺激的单核细胞对Daudi B细胞淋巴瘤的细胞毒性显著更强。流式细胞术显示,M-CSF使Fcγ受体III和I的单核细胞表达增加了1.6倍和1.5倍,而Fcγ受体II的表达保持不变。这些结果表明,用M-CSF预处理可提高利妥昔单抗对难治性CD20(+)淋巴瘤的治疗效果。