{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE294nnn/GSE294456/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE294456"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell TCR Profiling in Left Atria Identifies Complement Pathway Involvement in Atrial Fibrillation","description":"Atrial fibrillation (AF) is the most prevalent arrhythmia and is strongly associated with stroke, heart failure, and increased mortality. However, the role of T cells in AF pathogenesis remains unclear. In this study, we aimed to characterize the detailed landscape and clonal expansion of T cells using single-cell TCR sequencing, and validate our findings via O-link proteomics in plasma. Analysis of left atrial tissues from eight AF patients identified five CD4+ T cells, six CD8+ T cells, and gamma delta T cells based on canonical gene expression markers. Notably, we observed clonal expansion of resident memory and cytotoxic T cells. CellChat analysis highlighted complement signaling–mediated interactions between T cells and fibroblasts. Furthermore, proteomics in plasma using the Olink platform confirmed enriched complement activation in non-paroxysmal AF compared to paroxysmal AF. These findings suggest that activation of complement pathway between T cells and fibroblasts contributes to atrial remodeling and may serve as a potential therapeutic target for AF.","dates":{"publication":"2026/04/01"},"accession":"GSE294456","cross_references":{"GSM":["GSM8906502","GSM8906501","GSM8906500","GSM8906499"],"GPL":["24676"],"GSE":["294456"],"taxon":["Homo sapiens"]}}