Cañas Carlos A, Castaño-Valencia Santiago, Castro-Herrera Fernando
Universidad Icesi, CIRAT, Centro de Investigación en Reumatología, Autoinmunidad y Medicina Traslacional, Cali, Colombia.
Unit of Rheumatology, Fundación Valle del Lili, Cali, Colombia.
J Transl Autoimmun. 2022 Jan 24;5:100146. doi: 10.1016/j.jtauto.2022.100146. eCollection 2022.
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.
有100多种自身免疫性疾病（AD），其在普通人群中的患病率很高，介于5%至8%之间。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因其高发病率和死亡率，仍然是全球人们最为关注的健康问题。新治疗策略的开发已成为一个研究热点。近年来，免疫系统细胞中存在的离子通道，关于其功能作用、基因中的突变后果以及阻断它们的不同方式，都是深入研究的课题。药理学阻断KV1.3通道可抑制人CD4效应记忆T细胞中的Ca2+信号传导、T细胞增殖和促炎细胞因子的产生。这些细胞介导了大多数自身免疫性疾病，对它们的抑制是一个有前景的治疗靶点。在这篇综述中，我们将重点介绍KV1.3通道在T细胞中的生物学功能、药理学抑制（通过海葵和蝎子毒素、合成肽、纳米颗粒或单克隆抗体）的后果以及在自身免疫性疾病中的可能治疗应用。
