Laboratory of Alternative Medicine and Experimental Therapeutics, Department of Clinical Pharmacy, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Ishikawa 920-1181, Japan.
J Neuroimmunol. 2013 Apr 15;257(1-2):102-6. doi: 10.1016/j.jneuroim.2012.12.010. Epub 2013 Jan 11.
Autoantibody against nicotinic acetylcholine receptor (nAChR) α3 subunit has been implicated in the pathogenesis of paraneoplastic neurological syndrome. To examine the effect of anti-α3 subunit autoantibody on cell-surface nAChRs, we established human embryonic kidney 293 cells stably co-expressing α3 and β4 subunits. Upon incubation with seropositive patient's serum, this cell line showed co-accumulation of patient's IgG and α3 subunits in the cytoplasm. These data support the hypothesis that anti-α3 subunit autoantibody induces internalization of cell-surface nAChRs and thereby impairs synaptic transmission.
自身抗体针对烟碱型乙酰胆碱受体（nAChR）α3 亚单位已被牵连到副肿瘤性神经系统综合征的发病机制中。为了研究抗-α3 亚单位自身抗体对细胞表面 nAChR 的影响，我们建立了稳定共表达α3 和β4 亚单位的人胚肾 293 细胞。与血清阳性患者孵育后，该细胞系显示患者 IgG 和α3 亚单位在细胞质中的共聚集。这些数据支持这样一种假说，即抗-α3 亚单位自身抗体诱导细胞表面 nAChR 的内化，从而损害突触传递。
