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Analysis of various histone marks that regulate gene expression in response to pathogens identified H3K27me3 demethylation as an early NFAT5-dependent mechanism that facilitates p65 recruitment to promoters of various TLR4-induced genes. Altogether, these results advance our understanding about specific mechanisms that optimize antipathogen responses to limit infections.Low-grade inflammatory monocytes critically contribute to the pathogenesis of chronic inflammatory diseases such as atherosclerosis. The elevated expression of coactivati