Balaian Larisa, Ball Edward D
Department of Medicine and Cancer Center, University of California, San Diego School of Medicine, La Jolla, CA, USA.
Leuk Res. 2004 Aug;28(8):821-9. doi: 10.1016/j.leukres.2003.12.001.
Bi-specific anti-CD33 x anti-CD64 antibodies (BsAb) mediated more potent and longer-lasting inhibition of proliferation of human leukemia cell lines and primary acute myeloid leukemia (AML) samples compared to mono-specific anti-CD33 mAb. There were no differences between these two antibodies in cellular internalization over time. The inhibitory effect of BsAb was mimicked by a mouse IgG2a subclass mono-specific anti-CD33 mAb. These findings indicate that enhanced inhibition of proliferation was caused by simultaneous ligation of both CD33 and CD64 molecules. We conclude that inhibition of leukemia cell growth initiated by BsAb during prolonged exposure may have therapeutic value for the treatment of AML.
与单特异性抗CD33单克隆抗体相比,双特异性抗CD33×抗CD64抗体(BsAb)对人白血病细胞系和原发性急性髓系白血病(AML)样本的增殖具有更强且更持久的抑制作用。随着时间推移,这两种抗体在细胞内化方面没有差异。BsAb的抑制作用可被小鼠IgG2a亚类单特异性抗CD33单克隆抗体模拟。这些发现表明,对增殖的增强抑制是由CD33和CD64分子的同时连接引起的。我们得出结论,在长时间暴露期间,BsAb引发的白血病细胞生长抑制可能对AML治疗具有治疗价值。