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. 2021 Oct 7;12:756548. doi: 10.3389/fimmu.2021.756548

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Copyright © 2021 Toren, Burnette, Banerjee, Hunter and Tse

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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Steps of beta-cell death in T1D. Metabolic demand of nutrient challenge results in ER and oxidative stress (1) followed by chemokine release by the beta-cell (2). Chemokines attract immune cells (3), such as macrophages and T cells, which can damage the islet (4) directly though T cell interactions and indirectly through the release of inflammatory cytokines and reactive oxygen species. Cellular damage exacerbates ER and oxidative stress perpetuating this cycle. The inability to restore cellular homeostasis will result in beta-cell death (5).