{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE317nnn/GSE317990/"]},"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=GSE317990"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Translation factor eIF4G2 directs CD8⁺ T cell lineage commitment by selectively enabling the IL-7 receptor response","description":"Faithful CD8+ T cell lineage commitment depends on sustained IL-7 receptor (IL-7R) signaling. Here, we identify the translation initiation factor eIF4G2 as a specific and essential regulator of this process. Conditional deletion of Eif4g2 in CD4-expressing thymocytes specifically abrogated the expression of the shared IL-7R γ chain (γc) in a 5'/3'-UTR-dependent manner. This was accompanied by reduced expression of IL-7R α chain. The resultant collapse of the IL-7R complex ablated IL-7 signaling, thereby blocking CD8+ lineage commitment. This defect was selective, with TCR signaling and other cytokine receptors remaining intact. Our work establishes that eIF4G2 governs the thymic IL-7R axis and reveals a paradigm whereby a translational factor specifically tunes a key cytokine niche to direct T cell fate.","dates":{"publication":"2026/02/27"},"accession":"GSE317990","cross_references":{"GSM":["GSM9484087","GSM9484090","GSM9484089","GSM9484088"],"GPL":["28330"],"GSE":["317990"],"taxon":["Mus musculus"],"PMID":["[41940334]"]}}