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. 2020 Mar 12;11:119. doi: 10.3389/fendo.2020.00119

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Copyright © 2020 Pang, Luo, Huang, Xia, Xie and Zhou.

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) and the copyright owner(s) 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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Innate immunity (especially the type 1 IFN signaling pathway) and cytokine-induced apoptosis together contribute to beta-cell death. (1) When PAMPs are bound by PRRs, including the cytosolic receptors RIG-1 and MDA5 and endosomal TLRs, the interactions can promote the synthesis and secretion of type 1 IFNs. IFN-α/β bind their receptor IFNAR and induce the production of cytokines and chemokines that can cause and worsen insulitis and apoptosis. (2) The signaling pathways underlying cytokine-induced apoptosis mainly include (i) JAK/STAT signaling induced by IFN-γ binding to its receptor IFNGR and (ii) NF-κB and MAPK signaling induced by IL-β/IL-R and TNF-α/TNFR.