{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Csv":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE296nnn/GSE296401/suppl/GSE296401_CHD1_2D2_EAE_CNS.csv.gz","ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE296nnn/GSE296401/suppl/GSE296401_GR_2D2_EAE_CNS.csv.gz","ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE296nnn/GSE296401/suppl/GSE296401_CHD1_2D2_EAE_dLN.csv.gz","ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE296nnn/GSE296401/suppl/GSE296401_IL23R_WT_KO_Ctrl_Dex.csv.gz"],"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE296nnn/GSE296401/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE296401"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Interleukin-23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity II","description":"Interleukin-23 receptor (IL-23R) signaling is critical for the generation of pro-inflammatory CD4+ IL-17-producing T cells (Th17) that can drive autoimmune tissue inflammation, but the underlying mechanisms are not clear. We integrated phosphoproteomic and transcriptomic data downstream of IL-23R and IL-12R, which share a common subunit, to identify mechanisms engaged specifically by IL-23. We identified chromodomain helicase DNA-binding protein 1 (CHD1), an epigenetic regulator, and the glucocorticoid receptor (GR), a transcription factor (TF), as mediators of IL-23R signaling. IL-23R activation promoted CHD1 interaction with TF STAT3 and co-binding at the TF RORγt locus to enforce a pro-inflammatory Th17 state. Conversely, IL-23R signaling altered phosphorylation of the GR, thereby preventing its activation and nuclear translocation, ultimately impairing GR-driven inhibition of pro-inflammatory Th17 gene programs. Our findings uncover two mechanisms by which IL-23 promotes a pro-inflammatory Th17 cell state, offering potential therapeutic targets for treating Th17-driven autoimmune tissue inflammation and restoring homeostasis.","dates":{"publication":"2026/06/12"},"accession":"GSE296401","cross_references":{"GSM":["GSM8969703","GSM8969669","GSM8969702","GSM8969688","GSM8969666","GSM8969687","GSM8969668","GSM8969701","GSM8969700","GSM8969689","GSM8969667","GSM8969684","GSM8969683","GSM8969686","GSM8969685","GSM8969680","GSM8969682","GSM8969681","GSM8969677","GSM8969699","GSM8969698","GSM8969676","GSM8969679","GSM8969678","GSM8969695","GSM8969673","GSM8969694","GSM8969672","GSM8969697","GSM8969675","GSM8969674","GSM8969696","GSM8969691","GSM8969690","GSM8969671","GSM8969693","GSM8969692","GSM8969670"],"GPL":["19057","21626"],"GSE":["296401"],"taxon":["Mus musculus"]}}