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

• Published in: Journal of neuroimmunology Vol. 257; no. 1; pp. 102 - 106
• Main Authors: Kobayashi, Shota, Yokoyama, Shigeru, Maruta, Takahiro, Negami, Masako, Muroyama, Akiko, Mitsumoto, Yasuhide, Iwasa, Kazuo, Yamada, Masahito, Yoshikawa, Hiroaki
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 15.04.2013
• Subjects: Allergy and Immunology; Animals; Autoantibodies - physiology; Autoantibody; Cercopithecus aethiops; COS Cells; Endocytosis - immunology; Gene Expression Regulation - immunology; HEK293 Cells; Humans; Neurology; Nicotinic acetylcholine receptor α3 subunit; Rats; Receptor internalization; Receptors, Nicotinic - metabolism; Receptor internalization; Autoantibody; Nicotinic acetylcholine receptor α3 subunit
• ISSN: 0165-5728; 1872-8421
• DOI: 10.1016/j.jneuroim.2012.12.010

Abstract 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.