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

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

Author information

1
Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO, 80045, USA.
2
Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO, 80045, USA. Aaron.Michels@ucdenver.edu.

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.

KEYWORDS:

Autoimmunity; Clinical trials; Diabetes; Intervention; Prevention; Type 1

PMID:
27558810
DOI:
10.1007/s11892-016-0793-8
[Indexed for MEDLINE]

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