Disruption of FOXP3-EZH2 Interaction Represents a Pathobiological Mechanism in Intestinal Inflammation.

Forkhead box protein 3 (FOXP3) regulatory T cell (Treg) dysfunction is associated with autoimmune diseases; however， the mechanisms responsible for inflammatory bowel disease pathophysiology are poorly understood. Here， we tested the hypothesis that a physical interaction between transcription factor FOXP3 and the epigenetic enzyme enhancer of zeste homolog 2 (EZH2) is essential for gene co-repressive function.

C232， cysteine 232，CD， Crohn’s disease，ChIP， chromatin-immunoprecipitation，Crohn’s Disease，EED， embryonic ectoderm development，EZH2， enhancer of zeste homolog 2，Epigenetics，FCS， fetal calf serum，FOXP3， forkhead domain-containing X-chromosome–encoded protein，H3K27me3， trimethylated histone H3 at lysine 27，IBD， inflammatory bowel disease，IL， interleukin，IPEX， immune dysregulation， polyendocrinopathy， enteropathy， X-linked，JAK， Janus kinase，LZ， leucine zipper，PBMC， peripheral blood mononuclear cell，PBS， phosphate-buffered saline，PLA， proximity ligation assay，PMA， phorbol 12-myristate 13-acetate，PRC2， polycomb repressive complex 2，Proinflammatory Cytokine，Regulatory T Cells，STAT， signal transducer and activator of transcription，SUZ12， suppressor of zeste，Th， T helper，Treg， regulatory T cell，WT， wild-type，co-IP， co-immunoprecipita