Dissecting PGE2-driven inhibition of T cell activation using single-cell multi-omic and inflammatory bowel disease genetic association analysis

broadly suppressed T cell activation, except in Th17 and T follicular helper cells, and markedly altered chromatin accessibility and gene expression, particularly in Th17, Th1, and regulatory T cells, where IBD-associated SNPs were enriched in open chromatin and connected to cell type-specific cis-regulatory elements. Our study demonstrates the utility of single-cell multi-omics for defining stimulus-specific effects on T cells and prioritizing disease-associated genes.