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. 2015 Sep 14;6:134. doi: 10.3389/fendo.2015.00134

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Copyright © 2015 Hammerstad, Grock, Lee, Hasham, Sundaram and Tomer.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanisms by which IFNα affects beta cells to trigger islet autoimmunity. PDCs produce IFNα in response to infection. Binding to IFN type I receptor, IFNα or therapeutic IFNα, activates Jak/STAT pathways – inducing transcription of IFN-inducible genes leading to (1) production of proinflammatory cytokines, (2) increase expression of HLA class I, (3) stimulation of cytotoxic T cells. IFNα also induces ER stress, and epigenetic modification of genes involved in the pathogenesis of type 1 diabetes.