Gasque P, Thomas A, Fontaine M, Morgan B P
Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, UK.
J Neuroimmunol. 1996 May;66(1-2):29-40. doi: 10.1016/0165-5728(96)00015-x.
Two human neuroblastoma cell lines activated the classical pathway of complement in serum. Activation caused the opsonisation of these cells with complement fragments but with moderate cell killing. Neuroblastoma expressed regulators MCP and CD59 but did not express DAF or CR1. Neutralisation of CD59 rendered the cells susceptible to killing. Neuroblastoma also expressed C1-inhibitor, factor H, clusterin and S-protein. Expression of several regulators was enhanced by incubation with cytokines. Complement inhibition using soluble CRI markedly reduced opsonisation and killing of neuroblastoma. Our results suggest that complement might play a role in neuronal loss and that treatment with complement inhibitors might be of therapeutic value.
两种人类神经母细胞瘤细胞系激活了血清中的补体经典途径。激活导致这些细胞被补体片段调理,但细胞杀伤作用中等。神经母细胞瘤表达调节蛋白MCP和CD59,但不表达DAF或CR1。中和CD59使细胞易于被杀伤。神经母细胞瘤还表达C1抑制因子、因子H、簇集素和S蛋白。几种调节蛋白的表达通过与细胞因子孵育而增强。使用可溶性CRI抑制补体可显著降低神经母细胞瘤的调理作用和杀伤作用。我们的结果表明补体可能在神经元丢失中起作用,并且用补体抑制剂治疗可能具有治疗价值。