Autoantibody-induced internalization of nicotinic acetylcholine receptor α3 subunit exogenously expressed in human embryonic kidney cells

被引:14
|
作者
Kobayashi, Shota [1 ,2 ]
Yokoyama, Shigeru [3 ]
Maruta, Takahiro [4 ]
Negami, Masako [5 ]
Muroyama, Akiko [1 ]
Mitsumoto, Yasuhide [1 ]
Iwasa, Kazuo [6 ]
Yamada, Masahito [6 ]
Yoshikawa, Hiroaki [2 ,6 ]
机构
[1] Hokuriku Univ, Lab Alternat Med & Expt Therapeut, Dept Clin Pharm, Fac Pharmaceut Sci, Kanazawa, Ishikawa 9201181, Japan
[2] Kanazawa Univ, Hlth Serv Ctr, Kanazawa, Ishikawa 9201192, Japan
[3] Kanazawa Univ, Grad Sch Med, Dept Biophys Genet, Kanazawa, Ishikawa 9208640, Japan
[4] Kanazawa Nishi Hosp, Neurol Ctr, Kanazawa, Ishikawa 9200025, Japan
[5] Keiju Med Ctr, Nanao, Ishikawa 9268605, Japan
[6] Kanazawa Univ, Grad Sch Med Sci, Dept Neurol & Neurobiol Aging, Kanazawa, Ishikawa 9200025, Japan
关键词
Nicotinic acetylcholine receptor alpha 3 subunit; Autoantibody; Receptor internalization; AUTONOMIC NEUROPATHY; NEURONS;
D O I
10.1016/j.jneuroim.2012.12.010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Autoantibody against nicotinic acetylcholine receptor (nAChR) alpha 3 subunit has been implicated in the pathogenesis of paraneoplastic neurological syndrome. To examine the effect of anti-alpha 3 subunit autoantibody on cell-surface nAChRs, we established human embryonic kidney 293 cells stably co-expressing alpha 3 and beta 4 subunits. Upon incubation with seropositive patient's serum, this cell line showed co-accumulation of patient's IgG and alpha 3 subunits in the cytoplasm. These data support the hypothesis that anti-alpha 3 subunit autoantibody induces internalization of cell-surface nAChRs and thereby impairs synaptic transmission. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:102 / 106
页数:5
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