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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Tumor necrosis factor alpha (TNF-alpha), anti-TNF-alpha and demyelination revisited: an ongoing story.
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Tumor necrosis factor alpha (TNF-alpha), anti-TNF-alpha and demyelination revisited: an ongoing story.

机译:再次探讨了肿瘤坏死因子α(TNF-alpha),抗TNF-α和脱髓鞘作用。

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摘要

Tumor necrosis factor alpha (TNF-alpha) is a cytokine with pleiotropic actions that can be present both as a transmembrane protein and soluble cytokine (sTNF). Both ligands interact with two different receptors, TNFR1 and TNFR2, which mediate their biological effects. TNF-alpha is involved in the pathogenesis of multiple sclerosis (MS), however, administration of anti-TNF-alpha agents to MS patients has been associated with increased disease activity. Insomuch as TNFR1 mediates demyelination and TNFR2 remyelination, it could be hypothesized that anti-TNF-alpha agents which selectively inhibit sTNF or signals from TNFR1 could be effective in treating MS.
机译:肿瘤坏死因子α(TNF-alpha)是一种具有多效作用的细胞因子,可以以跨膜蛋白和可溶性细胞因子(sTNF)的形式出现。两种配体均与两个不同的受体TNFR1和TNFR2相互作用,从而介导它们的生物学效应。 TNF-α参与了多发性硬化症(MS)的发病机理,但是,向MS患者服用抗TNF-α药物与疾病活动性增加有关。由于TNFR1介导脱髓鞘和TNFR2的再髓鞘化,因此可以假设选择性抑制sTNF或TNFR1信号的抗TNF-α药物可有效治疗MS。

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