药物阻断KV1.3通道作为自身免疫性疾病的一种有前景的治疗方法

IF 4.7 Q2 IMMUNOLOGY
Carlos A. Cañas , Santiago Castaño-Valencia , Fernando Castro-Herrera
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引用次数: 8

摘要

有100多种自身免疫性疾病(AD),患病率很高,占总人口的5%至8%。1型糖尿病、多发性硬化症、系统性红斑狼疮和类风湿性关节炎由于其高发病率和死亡率,仍然是全世界人们最关注的健康问题。开发新的治疗策略已成为研究热点。近年来,对免疫系统细胞中存在的离子通道的研究,其功能作用、基因突变的后果以及阻断它们的不同方法是研究的热点。药物阻断KV1.3通道抑制人CD4+效应记忆T细胞中Ca2+信号,T细胞增殖和促炎白介素的产生。这些细胞介导了大部分阿尔茨海默病,它们的抑制是一个有希望的治疗靶点。在这篇综述中,我们将重点介绍T细胞中KV1.3通道的生物学功能,药物抑制的后果(通过海葵和蝎子毒素,合成肽,纳米颗粒或单克隆抗体)以及AD可能的治疗应用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Pharmacological blockade of KV1.3 channel as a promising treatment in autoimmune diseases

Pharmacological blockade of KV1.3 channel as a promising treatment in autoimmune diseases

There are more than 100 autoimmune diseases (AD), which have a high prevalence that ranges between 5% and 8% of the general population. Type I diabetes mellitus, multiple sclerosis, systemic lupus erythematosus and rheumatoid arthritis remain the health problem of highest concern among people worldwide due to its high morbidity and mortality. The development of new treatment strategies has become a research hotspot. In recent years, the study of the ion channels presents in the cells of the immune system, regarding their functional role, the consequences of mutations in their genes and the different ways of blocking them are the subject of intense research. Pharmacological blockade of KV1.3 channel inhibits Ca2+ signaling, T cell proliferation, and pro-inflammatory interleukins production in human CD4+ effector memory T cells. These cells mediated most of the AD and their inhibition is a promising therapeutic target. In this review, we will highlight the biological function of KV1.3 channel in T cells, consequence of the pharmacological inhibition (through anemone and scorpion toxins, synthetic peptides, nanoparticles, or monoclonal antibodies) as well as the possible therapeutical application in AD.

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来源期刊
Journal of Translational Autoimmunity
Journal of Translational Autoimmunity Medicine-Immunology and Allergy
CiteScore
7.80
自引率
2.60%
发文量
33
审稿时长
55 days
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