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Sci Transl Med:新研究试图通过改变免疫系统预防糖尿病发生!

2018-01-05 佚名 medicalxpress

科学家发现了一种机制,在进展为临床1型糖尿病之前,在胰岛自身免疫的早期阶段放大了自身免疫反应。如果研究人员阻断了相应的分子,免疫系统的活性显著下降。该研究是在德国糖尿病研究中心(DZD)的主持下进行的,并发表在“科学转化医学”杂志上。

科学家发现了一种机制,在进展为临床1型糖尿病之前,在胰岛自身免疫的早期阶段放大了自身免疫反应。如果研究人员阻断了相应的分子,免疫系统的活性显著下降。该研究是在德国糖尿病研究中心(DZD)的主持下进行的,并发表在“科学转化医学”杂志上。

1型糖尿病儿童和青少年中最常见的代谢疾病。在这种疾病中,人体自身的免疫系统会攻击和破坏胰腺产生胰岛素的细胞。调节性T细胞(Tregs)在这个过程中扮演着重要的角色:在健康的人,他们抑制过度的免疫反应,从而预防自身免疫性疾病。

Carolin Daniel博士的研究小组正在研究为什么Tregs不能保护1型糖尿病的胰岛细胞。她是Helmholtz ZentrumMünchen糖尿病研究所(IDF)的组长,也是DZD的科学家。在目前的研究中,她和她的团队阐明了一种机制,在胰岛自身免疫发病期间产生更少的Tregs,从而使免疫系统失控和攻击。

根据研究结果,miRNA181a和NFAT5分子起着关键作用。丹尼尔说:“我们发现miRNA181a导致胰岛自身免疫发病期间转录因子NFAT5的激活。 “结果是抑制了Treg的诱导,从而增加了免疫激活。”

为了测试这种新发现对于可能的治疗方法的适用性,由第一作者Isabelle Serr领导的科学家们研究了具有早期胰岛自身免疫的临床前模型。如果研究人员打断了miRNA181a / NFAT5轴,他们观察到免疫系统的激活显著降低,Tregs形成增加。这是通过miRNA181a以及NFAT5的药理学抑制实现的。

IDF主任Anette-Gabriele Ziegler教授说:“miRNA181a或NFAT5的靶向抑制可以开创新的方法来降低免疫系统对自身胰岛细胞的活性。 “与其他免疫调节治疗方法的结合也可以作为干预措施。”

未来,科学家们希望在临床前试验中进一步研究这些发现。为此,将使用人源化模型来测试胰岛素疫苗接种和miRNA181a / NFAT5轴抑制的组合是否导致对胰岛素产生细胞的更宽容的免疫系统。

原始出处:

Isabelle Serr, Martin G. Scherm, Adam M. Zahm, et.al. A miRNA181a/NFAT5 axis links impaired T cell tolerance induction with autoimmune type 1 diabetes. Science Translational Medicine  03 Jan 2018

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    2018-01-31 bsmagic9140
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    2018-01-05 changjiu

    学习一下持续

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Diabetic Med:糖尿病和职业伤害风险也有关?

近日,国际杂志 《Diabetic Med》上在线发表一项关于糖尿病和职业伤害风险的队列研究。目的是调查糖尿病是否与职业(工作场所或上下班)受伤的风险相关。 研究人员采用来自芬兰处方登记册的在2004年在大量雇员队列数据用于(芬兰公共部门研究)确定糖尿病病例。这些数据与从意外保险机构联合会获得的损伤记录相关联。总共1020例糖尿病病例(中位数年龄52岁,范围20至65岁; 66%的女性)及其

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