Immunobiology of myasthenia gravis, experimental autoimmune myasthenia gravis, and Lambert-Eaton syndrome.

Immunobiology of myasthenia gravis, experimental autoimmune myasthenia gravis, and Lambert-Eaton syndrome.
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重症肌无力的免疫生物学、实验性自身免疫性重症肌无力和兰伯特-伊顿综合征。

DOI:
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发表时间:
1985
影响因子:
29.7
通讯作者:
J. Lindstrom
J. Lindstrom
中科院分区:
医学1区
文献类型:
--
作者:
J. Lindstrom

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这种疾病的特征是肌肉无力和过度疲劳,现在被称为重症肌无力(MG),最初由Thomas Willis在1672年描述(1)。1973年,研究表明,用从鱼类电子器官中提纯的乙酰胆碱受体免疫兔子,也会引起类似的症状[2]。在接下来的十年里,研究人员证明,MG和实验性自身免疫性重症肌无力(EAMG)的症状都是由抗体介导的对乙酰胆碱受体的自身免疫反应(3-56)引起的。虽然我们现在对这种自身免疫反应损害神经肌肉传递的复杂机制有了合理的了解,但我们仍然不知道是什么启动和调节了MG的这种反应,也不知道与之相关的胸腺瘤的意义。虽然使用乙酰胆碱酯酶抑制剂(增加乙酰胆碱浓度和持续时间以补偿功能性受体的丧失)可以部分缓解肌肉无力,尽管胸腺切除术(7,8)、免疫抑制药物(9,10)和血浆置换(11,12)是有益的治疗方法,但对MG没有治愈方法。EAMG的发现是乙酰胆碱受体最初纯化的副产品。烟碱型乙酰胆碱受体目前为止
The muscular weakness and excessive fatigability that characterize the disease now known as myasthenia gravis (MG) were initially described by Thomas Willis in 1672 (1). In 1973 it was shown that immunization of rabbits with acetylcholine receptors purified from fish electric organs caused similar symptoms (2). During the following decade, researchers demonstrated that the symptoms of both MG and experimental autoim­ mune myasthenia gravis (EAMG) are caused by an antibody-mediated autoimmune response to acetylcholine receptors (3-56). Although we now have a reasonable understanding of the complex mechanisms by which this autoimmune response impairs neuromuscular transmission, we still do not know either what initiates and regulates this response in MG or the significance of the thymoma frequently associated with it. Although muscular weakness can be partially alleviated by treatment with inhibitors of acetylcholinesterase (which increase the concentration and duration of acetylcholine to compensate for the loss of functional receptors) and although thymectomy (7, 8), immunosuppressive drugs (9, 10), and plasmapheresis (11, 12) are beneficial therapies, there is no cure for MG. The discovery of EAMG was a by-product of the initial purification of acetylcholine receptors. Nicotinic acetylcholine receptors are now by far
通过体内外部伽马计数估计乙酰胆碱受体的降解率。
DOI: --
发表时间: 1982
期刊: Mayo Clinic proceedings. Mayo Clinic
影响因子: --
作者:
Fumagalli,G;Engel,AG;Lindstrom,J
通讯作者: Lindstrom,J
针对乙酰胆碱受体胞质结构域的单克隆抗体。
DOI: --
发表时间: 1983
期刊: The Journal of biological chemistry
影响因子: --
作者:
Froehner,SC;Douville,K;Klink,S;Culp,WJ
通讯作者: Culp,WJ
使用单克隆抗体研究来自电器官、肌肉和大脑的乙酰胆碱受体以及重症肌无力受体的自身免疫反应。
DOI: 10.1101/sqb.1983.048.01.012
发表时间: 1983
期刊: Cold Spring Harbor symposia on quantitative biology
影响因子: --
作者:
Lindstrom,J;Tzartos,S;Gullick,W;Hochschwender,S;Swanson,L;Sargent,P;Jacob,M;Montal,M
通讯作者: Montal,M
DOI: 10.1101/sqb.1983.048.01.003
发表时间: 1983
期刊: Cold Spring Harbor symposia on quantitative biology
影响因子: --
作者:
Karlin,A;Cox,R;Kaldany,RR;Lobel,P;Holtzman,E
通讯作者: Holtzman,E
实验性自身免疫性重症肌无力中的淋巴细胞激活。
DOI: --
发表时间: 1982
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
DeBaets,MH;Einarson,B;Lindstrom,JM;Weigle,WO
通讯作者: Weigle,WO