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1型糖尿病中的免疫干预与胰岛β细胞功能的保护

Immune Intervention and Preservation of Pancreatic Beta Cell Function in Type 1 Diabetes.

作者信息

Simmons Kimber M, Gottlieb Peter A, Michels Aaron W

机构信息

Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO, 80045, USA.

出版信息

Curr Diab Rep. 2016 Oct;16(10):97. doi: 10.1007/s11892-016-0793-8.

Abstract

Type 1 diabetes (T1D) results from the immune-mediated destruction of insulin-producing β cells located within the pancreatic islets of Langerhans. The autoimmune process leads to a deficiency in insulin production and resultant hyperglycemia requiring lifelong treatment with insulin administration. T1D continues to dramatically increase in incidence, especially in young children. Substantial knowledge surrounding human disease pathogenesis exists, such that T1D is now predictable with the measurement of antibodies in the peripheral blood directed against insulin and other β cell proteins. With the ability to predict, it naturally follows that T1D should be preventable. As such, over the last two decades, numerous well-controlled clinical trials have been completed attempting to prevent diabetes onset or maintain residual β cell function after clinical onset, all providing relatively disappointing results. Here, we review the T1D prevention efforts, the current landscape of clinical therapies, and end with a discussion regarding the future outlook for preventing T1D.

摘要

1型糖尿病(T1D)是由位于胰岛的胰岛素分泌β细胞受到免疫介导破坏所致。自身免疫过程导致胰岛素分泌不足,进而引发高血糖,需要终身注射胰岛素进行治疗。T1D的发病率持续急剧上升,尤其是在幼儿中。目前对人类疾病发病机制已有相当多的了解,以至于现在通过检测外周血中针对胰岛素和其他β细胞蛋白的抗体就能预测T1D。既然能够预测,那么T1D自然应该是可预防的。因此,在过去二十年里,已经完成了许多严格控制的临床试验,试图预防糖尿病的发生或在临床发病后维持残余β细胞功能,但所有试验结果都相对令人失望。在此,我们回顾了预防T1D的努力、临床治疗的现状,并最后讨论了预防T1D的未来前景。

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