Balaian L, Ball E D
Department of Medicine and Cancer Center, University of California, San Diego School of Medicine, La Jolla, CA 92093-0960, USA.
Leuk Res. 2001 Dec;25(12):1115-25. doi: 10.1016/s0145-2126(01)00084-4.
Bispecific anti-CD33 x anti-CD64 antibody (BsAb) directly inhibited proliferation and colony formation of human acute myeloid leukemia cell lines, without affecting the function of normal monocytes. Addition of BsAb to normal monocytes induced tyrosine phosphorylation of Cbl and Vav, association of these molecules with CD33, and downstream signaling. In leukemia cells that were insensitive to BsAb treatment, Vav and Cbl were constitutively phosphorylated and, therefore, constitutively associated with CD33. Direct growth inhibition is an additional mechanism by which BsAb may be useful in the therapy of AML.
双特异性抗CD33×抗CD64抗体（BsAb）可直接抑制人急性髓系白血病细胞系的增殖和集落形成，而不影响正常单核细胞的功能。向正常单核细胞中添加BsAb可诱导Cbl和Vav的酪氨酸磷酸化、这些分子与CD33的结合以及下游信号传导。在对BsAb治疗不敏感的白血病细胞中，Vav和Cbl持续磷酸化，因此持续与CD33结合。直接生长抑制是BsAb可能用于急性髓系白血病治疗的另一种机制。
