Spiller O B, Moretto G, Kim S U, Morgan B P, Devine D V
Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, UK.
J Neuroimmunol. 1996 Dec;71(1-2):97-106. doi: 10.1016/s0165-5728(96)00136-1.
Primary fetal human astrocytes and an astrocytoma cell line, U373-MG, expressed membrane cofactor protein (CD46), CD59, and low levels of decay-accelerating factor (CD55). Astrocyte CD55 was capable of regulating C3 deposition on the cell surface; albeit at a lower level than primary human fibroblasts. Negligible complement-mediated lysis of primary astrocytes and the U373-MG cell line was observed, even when large amount of astrocyte-specific, complement-activating antibodies were bound to the cells. Blocking the function of CD59 on astrocytes resulted in a > 90% cell lysis, while equivalent lysis of fibroblasts could only be achieved with additional blocking of CD55.
原代人胎儿星形胶质细胞和一种星形细胞瘤细胞系U373 - MG表达膜辅因子蛋白(CD46)、CD59和低水平的衰变加速因子(CD55)。星形胶质细胞的CD55能够调节C3在细胞表面的沉积;尽管其水平低于原代人成纤维细胞。即使大量星形胶质细胞特异性的补体激活抗体结合到细胞上,原代星形胶质细胞和U373 - MG细胞系的补体介导的裂解也可忽略不计。阻断星形胶质细胞上CD59的功能会导致> 90%的细胞裂解,而对于成纤维细胞,只有在额外阻断CD55的情况下才能实现同等程度的裂解。