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T-cell tumor necrosis factor-alpha receptor binding in myasthenic patients.

机译:重症肌无力患者中的T细胞肿瘤坏死因子-α受体结合。

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摘要

Myasthenia gravis (MG) is a T-cell-dependent and antibody-mediated autoimmune disease of the neuromuscular junction, in which the cytokine network may be deranged. Specific receptors for tumor necrosis factor (TNF)-alpha, a cytokine with several effects on the neuroimmune system, were found on human lymphocytes. In the present study, we assayed TNF-alpha binding on peripheral blood T-cells from MG patients, finding that T-cells from patients have significantly more TNF-alpha receptors than those from controls (Bmax: 654 +/- 12 vs. 133 +/- 4 (mean +/- SEM) receptors/cell). Such TNF-alpha binding sites are of the same type in patients and healthy subjects (Kd: 68.7 +/- 4.3 vs. 70.1 +/- 4.8 (mean +/- SEM) pM). The enhanced T-cell TNF-alpha binding is due to an increased number of TNF-alpha receptors on T-helper lymphocytes. These results are discussed in terms of MG immunopathogenesis, since it has been reported that activated T-cells have increased amounts of TNF-alpha receptors.
机译:重症肌无力(MG)是一种T细胞依赖性神经肌肉接头的抗体介导的自身免疫性疾病,其中细胞因子网络可能紊乱。在人类淋巴细胞上发现了肿瘤坏死因子(TNF)-α(一种对神经免疫系统有多种作用的细胞因子)的特异性受体。在本研究中,我们分析了MG患者外周血T细胞上的TNF-α结合,发现患者的T细胞比对照组的T细胞具有明显更多的TNF-α受体(Bmax:654 +/- 12 vs. 133 +/- 4(平均+/- SEM)受体/细胞)。所述TNF-α结合位点在患者和健康受试者中是相同类型的(Kd:68.7 +/- 4.3与70.1 +/- 4.8(平均+/- SEM)pM)。 T细胞TNF-α结合增强是由于T辅助淋巴细胞上的TNF-α受体数量增加。由于已经报道了活化的T细胞具有增加量的TNF-α受体,因此就MG免疫发病机理讨论了这些结果。

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