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重症肌无力患者外周血中CD5 + B淋巴细胞的频率。

The frequency of CD5+ B lymphocytes in the peripheral blood of patients with myasthenia gravis.

作者信息

Ragheb S, Lisak R P

机构信息

Department of Neurology, Wayne State University, Detroit, MI 48201.

出版信息

Neurology. 1990 Jul;40(7):1120-4. doi: 10.1212/wnl.40.7.1120.

DOI:10.1212/wnl.40.7.1120
PMID:1694020
Abstract

A subset of human B lymphocytes expresses Leu-1 (CD5), a pan-T cell marker, which is the equivalent of the murine Lyt-1 molecule. CD5+ B cells produce autoantibodies in vitro; therefore, they may play a role in the pathogenesis of autoimmune disorders. In myasthenia gravis (MG), autoantibodies are directed against the nicotinic acetylcholine receptor (AChR) at the neuromuscular junction. We examined the peripheral blood leukocytes of MG patients (n = 21) and controls (n = 15) for the presence of Leu-1+ B lymphocytes. A fraction of B-1 (CD20)+ cells expressed Leu-1 at a low density. There was a statistically significant difference in the frequency of Leu-1+ B cells between patients and controls. We observed 2 frequency ranges of Leu-1+ B cells (0 to 30% and above 30%), which were not related to the total percentage of B-1+ cells in the blood. Fifty-seven percent of MG patients had a high frequency of Leu-1+ B cells compared with 13% of controls.

摘要

人类B淋巴细胞的一个亚群表达Leu-1(CD5),这是一种全T细胞标志物,等同于小鼠的Lyt-1分子。CD5+B细胞在体外产生自身抗体;因此,它们可能在自身免疫性疾病的发病机制中起作用。在重症肌无力(MG)中,自身抗体针对神经肌肉接头处的烟碱型乙酰胆碱受体(AChR)。我们检测了MG患者(n = 21)和对照组(n = 15)外周血白细胞中Leu-1+B淋巴细胞的存在情况。一部分B-1(CD20)+细胞低密度表达Leu-1。患者和对照组之间Leu-1+B细胞的频率存在统计学显著差异。我们观察到Leu-1+B细胞有两个频率范围(0至30%和高于30%),这与血液中B-1+细胞的总百分比无关。与13%的对照组相比,57%的MG患者有高频率的Leu-1+B细胞。

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The frequency of CD5+ B lymphocytes in the peripheral blood of patients with myasthenia gravis.重症肌无力患者外周血中CD5 + B淋巴细胞的频率。
Neurology. 1990 Jul;40(7):1120-4. doi: 10.1212/wnl.40.7.1120.
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Synthesis of anti-acetylcholine receptor antibodies by CD5- B cells from peripheral blood of myasthenia gravis patients.重症肌无力患者外周血中CD5 - B细胞合成抗乙酰胆碱受体抗体。
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Clin Exp Immunol. 1995 Aug;101(2):346-50. doi: 10.1111/j.1365-2249.1995.tb08362.x.