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Immunology of acetylcholine receptors in relation to myasthenia gravis.

作者信息

Vincent A

出版信息

Physiol Rev. 1980 Jul;60(3):756-824. doi: 10.1152/physrev.1980.60.3.756.

DOI:10.1152/physrev.1980.60.3.756
PMID:6248907
Abstract
摘要

相似文献

1
Immunology of acetylcholine receptors in relation to myasthenia gravis.与重症肌无力相关的乙酰胆碱受体免疫学
Physiol Rev. 1980 Jul;60(3):756-824. doi: 10.1152/physrev.1980.60.3.756.
2
Electrophysiological studies of thymectomized and nonthymectomized acetylcholine receptor-immunized animal models of myasthenia gravis.
Exp Neurol. 1979 Jan;63(1):1-27. doi: 10.1016/0014-4886(79)90182-1.
3
Myasthenia gravis and autoimmunity.重症肌无力与自身免疫
Adv Intern Med. 1980;26:489-510.
4
Autoimmune myasthenia gravis.自身免疫性重症肌无力
Hosp Pract (Off Ed). 1993 Jan 15;28(1):109-12, 115-7, 121-2, passim. doi: 10.1080/21548331.1993.11442741.
5
Myasthenia gravis induced by monoclonal antibodies to acetylcholine receptors.抗乙酰胆碱受体单克隆抗体诱发的重症肌无力。
Nature. 1980 May 22;285(5762):238-40. doi: 10.1038/285238a0.
6
The role of humoral immunity in myasthenia gravis.
Prog Brain Res. 1979;49:435-40. doi: 10.1016/S0079-6123(08)64655-5.
7
Myasthenia gravis (first of two parts).重症肌无力(两部分中的第一部分)
N Engl J Med. 1978 Jan 19;298(3):136-42. doi: 10.1056/NEJM197801192980305.
8
[Pathogenesis and pathophysiology of myasthenia gravis--electrophysiological, ultrastructural and immunological aspects of neuromuscular junctions (author's transl)].重症肌无力的发病机制与病理生理学——神经肌肉接头的电生理、超微结构及免疫学方面(作者译)
No To Shinkei. 1980 Sep;32(9):891-908.
9
How the autoimmune response to acetylcholine receptor impairs neuromuscular transmission in myasthenia gravis and its animal model.自身免疫性抗乙酰胆碱受体反应如何损害重症肌无力及其动物模型中的神经肌肉传递。
Fed Proc. 1978 Dec;37(14):2828-30.
10
[Immunologic aspects of disorders of neuromuscular transmission. 2. Experimental autoimmune myasthenia gravis and the Lambert-Eaton myasthenic syndrome].[神经肌肉传递障碍的免疫学方面。2. 实验性自身免疫性重症肌无力和兰伯特-伊顿肌无力综合征]
Lijec Vjesn. 1994 May-Jun;116(5-6):158-61.

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Biological implications of thymectomy for myasthenia gravis.胸腺瘤切除术对重症肌无力的生物学意义。
Surg Today. 2010;40(2):102-7. doi: 10.1007/s00595-009-4134-2. Epub 2010 Jan 28.
2
Immunological function of thymoma and pathogenesis of paraneoplastic myasthenia gravis.胸腺瘤的免疫功能及副肿瘤性重症肌无力的发病机制。
Gen Thorac Cardiovasc Surg. 2008 Apr;56(4):143-50. doi: 10.1007/s11748-007-0185-8. Epub 2008 Apr 10.
3
Regulation of acetylcholine receptor gene expression in human myasthenia gravis muscles. Evidences for a compensatory mechanism triggered by receptor loss.
人类重症肌无力肌肉中乙酰胆碱受体基因表达的调控。受体丧失引发补偿机制的证据。
J Clin Invest. 1998 Jul 1;102(1):249-63. doi: 10.1172/JCI1248.
4
Effect of diazepam on muscle weakness in a model of myasthenia gravis in rats.
J Neural Transm Gen Sect. 1993;93(3):181-5. doi: 10.1007/BF01244995.
5
Ocular myasthenia gravis. A critical review of clinical and pathophysiological aspects.眼肌型重症肌无力。临床与病理生理学方面的批判性综述。
Doc Ophthalmol. 1993;84(4):309-33. doi: 10.1007/BF01215447.
6
Thymectomy and azathioprine have no effect on the phenotype of CD4 T lymphocyte subsets in myasthenia gravis.胸腺切除术和硫唑嘌呤对重症肌无力患者CD4 T淋巴细胞亚群的表型没有影响。
J Neurol Neurosurg Psychiatry. 1993 Jan;56(1):46-51. doi: 10.1136/jnnp.56.1.46.
7
Regulation of acetylcholine receptor alpha subunit variants in human myasthenia gravis. Quantification of steady-state levels of messenger RNA in muscle biopsy using the polymerase chain reaction.人类重症肌无力中乙酰胆碱受体α亚基变体的调控。使用聚合酶链反应对肌肉活检中信使核糖核酸的稳态水平进行定量分析。
J Clin Invest. 1994 Jul;94(1):16-24. doi: 10.1172/JCI117302.
8
Autoantibodies against eukaryotic protein L7 in patients suffering from systemic lupus erythematosus and progressive systemic sclerosis: frequency and correlation with clinical, serological and genetic parameters. The SLE Study Group.系统性红斑狼疮和进行性系统性硬化症患者中抗真核蛋白L7自身抗体:频率及其与临床、血清学和遗传参数的相关性。SLE研究组
Clin Exp Immunol. 1995 May;100(2):198-204. doi: 10.1111/j.1365-2249.1995.tb03653.x.
9
Myasthenia gravis: an autoimmune response against the acetylcholine receptor.重症肌无力:针对乙酰胆碱受体的自身免疫反应。
Immunol Res. 1993;12(1):78-100. doi: 10.1007/BF02918370.
10
Specific tolerance to an acetylcholine receptor epitope induced in vitro in myasthenia gravis CD4+ lymphocytes by soluble major histocompatibility complex class II-peptide complexes.可溶性主要组织相容性复合体II类-肽复合物在体外诱导重症肌无力CD4 +淋巴细胞产生对乙酰胆碱受体表位的特异性耐受。
J Clin Invest. 1994 Apr;93(4):1361-9. doi: 10.1172/JCI117112.