Researchers from the University of Pennsylvania and the HPAP Consortium identified a conserved transcriptional and epigenetic program in a subset of CD4 memory helper T cells associated with type 1 diabetes (T1D). Published in Science Immunology, the study profiled pancreatic lymph nodes and spleens from donors with T1D, autoantibody‑positive individuals, and controls, revealing cells with elevated NFKB1 and BACH2 expression and chromatin remodeling. The findings define candidate biomarkers and potential therapeutic targets for autoimmune islet destruction. The work pairs gene‑expression and chromatin‑accessibility profiling to map disease‑associated immune states.