<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/GSE306750/</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=GSE306750</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Spatial organization of pulmonary type 2 inflammation by a macrophage-derived cholesterol metabolite</name><description>Effective pulmonary immunity requires the precise spatial organization of immune cells, yet the mechanisms guiding their intratissue positioning during inflammation remain unclear. Here, we identify a cholesterol-derived chemotactic axis that spatially organizes T helper 2 (TH2) cells during fungal-induced pulmonary type 2 inflammation. Inflammation-expanded macrophages expressing cholesterol-25-hydroxylase (CH25H) produce 25-hydroxycholesterol, which is converted into the oxysterol 7α,25-dihydroxycholesterol to attract GPR183-expressing TH2 cells into inflammatory Ly6C+ macrophages, promoting fungal persistence. Disruption of this axis via TH2- specific GPR183 deletion restores type 1 macrophage activation and enhances fungal clearance. Our findings reveal a macrophage-driven, metabolite-based mechanism of immunosuppressive cell positioning in inflamed lung tissue.</description><dates><publication>2026/05/18</publication></dates><accession>GSE306750</accession><cross_references><GSM>GSM9207214</GSM><GSM>GSM9207215</GSM><GSM>GSM9207210</GSM><GSM>GSM9207211</GSM><GSM>GSM9207212</GSM><GSM>GSM9207213</GSM><GPL>19057</GPL><GSE>306750</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>