Multi-omics data compendium of pancreatic islet and β cell responses to pro-inflammatory cytokines

In type 1 diabetes (T1D), autoimmune responses and inflammation cause the death of pancreatic β cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)α, IFNγ, interleukin (IL)-1β, and tumor necrosis factor (TNF)α, which induce β-cell dysfunction and apoptosis. A deep understanding of the β-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/β-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq and ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in β-cell stress/death. Here, we aggregated 51 (multi-)omics datasets from 19 studies spanning 14 years into a centralized location, providing a quality-controlled, statistically rigorous resource for investigators seeking to holistically study the impact of pro-inflammatory cytokines on β-cell fate.