<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/GSE287nnn/GSE287431/</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> Genome binding/occupancy profiling by high throughput sequencing</gds_type><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE287431</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Brief high-fat diet exposure imprints TH17-driven inflammatory memory in skin independent of obesity</name><description>Obesity alters immune responses across inflammatory contexts; however, whether brief dietary changes influence immune function independent of weight gain remains unclear. Here, we demonstrate that transient high-fat diet (HFD) exposure during the onset of psoriasiform inflammation markedly exacerbates disease severity in lean mice. Mechanistically, HFD rapidly increases neutrophil accumulation and NLRP3-dependent IL-1β production in lesional skin, promoting IL-1R1⁺ pathogenic TH17 differentiation and establishment of a chromatin-primed tissue-resident memory CD4⁺ T cell population. Transient HFD exposure during disease onset durably amplifies inflammatory recall responses upon rechallenge, despite subsequent dietary normalization. These findings identify diet on disease onset (DODO) as a critical modifier of inflammatory disease trajectory. Single-nucleus ATAC-seq of CD4⁺ T cells from recovered skin following diet-modulated IMQ-induced inflammation Transient high-fat diet (HFD) exposure during the onset of psoriasiform inflammation induces durable transcriptional and epigenomic remodeling in CD4⁺ T cells. To define chromatin accessibility programs associated with inflammatory memory, we performed single-nucleus ATAC sequencing (snATAC-seq) of sorted CD4⁺ T cells isolated from ear skin following recovery from imiquimod (IMQ)-induced inflammation in mice fed either low-fat diet (LFD) or HFD. These data enable identification of differentially accessible regulatory elements and chromatin states associated with diet on disease onset (DODO)-driven inflammatory memory.</description><dates><publication>2026/08/06</publication></dates><accession>GSE287431</accession><cross_references><GSM>GSM8745588</GSM><GSM>GSM8745586</GSM><GSM>GSM9559624</GSM><GSM>GSM8745587</GSM><GSM>GSM9559625</GSM><GSM>GSM9540488</GSM><GPL>34328</GPL><GSE>287431</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>