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作 者:丁欣[1] 于洁[1] 闫晶[1] 吴迪宾[1] 张海鸥[1]
出 处:《中华神经医学杂志》2006年第7期689-691,共3页Chinese Journal of Neuromedicine
摘 要:目的研究副肿瘤综合征(PNS)自身抗体(抗Hu抗体)对培养神经细胞的直接影响。方法抗Hu抗体阳性PNS患者血清IgG、对照组血清IgG添加到由胎鼠脑分离出的培养神经细胞,观察有无细胞的凋亡。对照组血清IgG为:(1)AB型健康人标准血清;(2)无神经损害症状的抗Hu抗体阴性痛患者血清;(3)重组Hu蛋白吸附后的抗Hu抗体阳性患者血清。结果添加抗Hu抗体阳性PNS患者血清IgG的培养神经细胞互相融合,由粗而长的突起相互连接,而对照组未看到上述变化。各组均未发现凋亡的神经细胞。结论抗Hu抗体未能引起神经细胞的凋亡或死亡,推测是诱导了接触因子的表达促进了细胞的分化。Objective To examine the direct effects of the autoantibody (anti-Hu antibody) of paraneoplastic neurological syndrome on primary-cultured neurons. Methods The serum IgG from PNS patients with anti-Hu antibody and control groups cultured in mouse-brain-derived neurons to observe apoptosis respectively. The serum IgG of control groups came from (1)AB blood type of healthybodies; (2) cancer patients without neurological symptoms anti-Hu antibody negative; (3)antibodyabsorbed sera from Hu-IgG patients with Hu recombinant protein. Results Neurons incubated with Hu-IgG started to fuse and extended long and thick dendrites, which were not found in the control groups. No apoptotic neurons were found in each group. Conclusion Anti-Hu antibody did not kill neurons, but induced the expression of cell adhesion molecules and accelerated neuronal differentiation. Suggesting that anti-Hu antibody was not through the binding of the antibody to specific antigen, but in IgG fraction some other factors were contained.
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