{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE306nnn/GSE306684/"]},"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=GSE306684"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"E Protein-Driven iNKT Subset Modulation Shapes Early Immune Responses during Influenza A Virus Infection.","description":"IAV infection elicits a robust immune response including invariant natural killer T (iNKT) cells. Using mouse strains with normal iNKT numbers but altered subset representation (NKTWT vs NKTET-2), we show that NKTET-2 mice exhibit reduced weight loss, diminished neutrophil recruitment and inflammatory monocyte activation, and ~40% less HA+ infected lung area versus controls. Early lung expression of type I IFN–responsive genes (IFIT1, ISG15) and chemokines (CCL2, CXCL2) was lower in NKTET-2, whereas IFNλ was elevated. Single-cell RNA-seq of sorted lung iNKT cells revealed that NKTET-2 favored adhesion/repair and iNKT17-like programs over NKTWT type 1 effector responses. Modulating iNKT subset balance may limit immunopathology while preserving antiviral defense in IAV.","dates":{"publication":"2026/05/15"},"accession":"GSE306684","cross_references":{"GSM":["GSM9206180","GSM9206179"],"GPL":["34290"],"GSE":["306684"],"taxon":["Mus musculus"],"PMID":["[42089345]"]}}