<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE306nnn/GSE306684/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE306684</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>E Protein-Driven iNKT Subset Modulation Shapes Early Immune Responses during Influenza A Virus Infection.</name><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.</description><dates><publication>2026/05/15</publication></dates><accession>GSE306684</accession><cross_references><GSM>GSM9206180</GSM><GSM>GSM9206179</GSM><GPL>34290</GPL><GSE>306684</GSE><taxon>Mus musculus</taxon><PMID>[42089345]</PMID></cross_references></HashMap>