{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE299nnn/GSE299966/"]},"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=GSE299966"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"CXCR6+ CD4+ Tissue-Resident Memory T Cells Orchestrate Relapse in Allergic Dermatitis via CXCL16-Dependent Persistence","description":"The persistence of CD4+ tissue-resident memory T (TRM) cells is crucial for relapse in allergic skin conditions; however, the mechanisms underlying their maintenance and pathogenic potential remain poorly defined. Here, we identified CXCR6+ CD4+ TRM cells as a distinct pathogenic subset that rapidly induces relapse through cytokine production in allergic dermatitis. This subset requires CXCL16-dependent interactions with CD301b+ conventional dendritic cell subset 2 (cDC2) for in situ maintenance. Functional blockade of the CXCL16–CXCR6 signaling pathway attenuated local TRM proliferation and reduced antigen-induced relapse in murine models. In human atopic dermatitis (AD), CXCR6+ CD4+ TRM cells co-localized with CD301+ cDC2 in perivascular clusters even after successful anti-IL-13 therapy. These findings highlight CXCR6+ CD4+ TRM cells as a pathogenic reservoir sustaining chronic and recurrent inflammation, and propose the CXCL16–CXCR6 axis as a therapeutic target to prevent relapse in allergic skin diseases, such as AD.","dates":{"publication":"2026/10/01"},"accession":"GSE299966","cross_references":{"GSM":["GSM9051156","GSM9051154","GSM9051155","GSM9051153"],"GPL":["28457"],"GSE":["299966"],"taxon":["Mus musculus"]}}