当前位置： SCI文献检索 > JOURNAL OF NEUROIMMUNOLOGY期刊下所有文献 > Modulation of acetylcholine receptor function in TE671 (rhabdomyosarcoma) cells by non-AChR ligands: possible relevance to seronegative myasthenia gravis.

Modulation of acetylcholine receptor function in TE671 (rhabdomyosarcoma) cells by non-AChR ligands: possible relevance to seronegative myasthenia gravis.

Abstract：

:The acetylcholine receptor (AChR) is the main target antigen in myasthenia gravis (MG), but about 15% of patients with typical immunologically mediated MG do not have detectable anti-AChR antibodies. Previous studies showed that plasma from these 'seronegative' patients (SNMG) reduced AChR function in the human AChR-expressing TE671 cell line, and it was proposed that SNMG plasmas may act indirectly via phosphorylation of AChR. We show here that substances such as the beta 2-adrenergic agonist, salbutamol, calcitonin-gene-related-peptide (CGRP), and cholera toxin, that increase intracellular cAMP via binding to specific cell-surface receptors, reduced AChR function in TE671 cells. Moreover, non-specific activation of cell surface proteins by lectins achieved similar results. These observations lead us to hypothesise that SNMG immunoglobulins act in TE671 cells by cross-linking of specific cell surface antigen(s) resulting in generation of intracellular cAMP and/or other second messengers. The role of such antibodies at the neuromuscular junction in vivo could be reduction in AChR function by desensitization and/or damage to the postsynaptic membrane following complement activation.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Li Z,Forester N,Vincent A

doi

10.1016/0165-5728(95)00169-7

subject

Has Abstract

pub_date

1996-02-01 00:00:00

pages

179-83

issue

2

eissn

0165-5728

issn

1872-8421

pii

0165572895001697

journal_volume

64

pub_type

杂志文章

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