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J Autoimmun. 2016 Aug;72:118-25. doi: 10.1016/j.jaut.2016.05.009. Epub 2016 May 30.

Maintenance of peripheral tolerance to islet antigens.

Author information

1
The University of Queensland Diamantina Institute, University of Queensland, Translational Research Institute, Brisbane, QLD, Australia. Electronic address: e.hamiltonwilliams@uq.edu.au.
2
The University of Queensland Diamantina Institute, University of Queensland, Translational Research Institute, Brisbane, QLD, Australia.

Abstract

Reestablishment of immune tolerance to the insulin-producing beta cells is the desired goal for type 1 diabetes (T1D) treatment and prevention. Immune tolerance to multiple islet antigens is defective in individuals with T1D, but the mechanisms involved are multifaceted and may involve loss of thymic and peripheral tolerance. In this review we discuss our current understanding of the varied mechanisms by which peripheral tolerance to islet antigens is maintained in healthy individuals where genetic protection from T1D is present and how this fails in those with genetic susceptibility to disease. Novel findings in regards to expression of neo-islet antigens, non-classical regulatory cell subsets and the impact of specific genetic variants on tolerance induction are discussed.

KEYWORDS:

Genetic susceptibility; Regulatory T cells; Tolerance; Type 1 diabetes

PMID:
27255733
DOI:
10.1016/j.jaut.2016.05.009
[Indexed for MEDLINE]

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