{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE338nnn/GSE338460/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":[" Other","Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE338460"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Immune hallmarks of recurrent immune checkpoint inhibitor-mediated inflammatory arthritis","description":"Immune checkpoint inhibitor (ICI) therapy is often associated with immune-related adverse events including inflammatory arthritis (ICI-IA). However, the mechanisms underlying ICI-IA, especially its recurrence, have not been fully investigated. The purpose of this study is to elucidate mechanisms of recurrent ICI-IA by analyzing longitudinal synovial fluid (SF) samples. SF samples were collected from six ICI-IA patients at the first and second occurrences of ICI-IA and analyzed with single-cell RNA sequencing (scRNAseq) (n=3), scTCRseq (n=3), scBCRseq (n=3), and flow cytometry (n=6). SF samples from cancer-naïve osteoarthritis patients (n=6) were used as negative controls. Analysis revealed that effector CD8+ T cells and PD-1hi CXCL13hi CD4+ T cells were enriched in the SF of ICI-IA patients. Ninety three percent and fifty percent of the top ten expanded clones of effector CD8+ T cells and PD-1hi CXCL13hi CD4+ T cells, respectively, were shared between the first and second ICI-IA flare. These top clones were characterized by the production of pro-inflammatory type 1 cytokines including IFNg, TNFa, and IL-21, especially in the second flare, suggesting immune memory responses to cognate antigen. Cell-cell communication analysis suggests that effector CD8+ T cells and PD-1hi CXCL13hi CD4+ T cells interacted with each other and with myeloid cells and B cells through chemokines (CXCL9/10/11/13, CCL3) and cytokines (MIF, IL-2/7/15/21). Overall, longitudinal SF analysis from ICI-IA patients for the first time revealed the expansion of effector CD8+ T cells and PD-1hi CXCL13hi CD4+ T cells with type 1 cytokine signatures that potentially contribute to development or recurrence of ICI-IA.","dates":{"publication":"2026/07/25"},"accession":"GSE338460","cross_references":{"GSM":["GSM9874766","GSM9874767","GSM9874764","GSM9874765","GSM9874768","GSM9874769","GSM9874780","GSM9874781","GSM9874762","GSM9874763","GSM9874760","GSM9874782","GSM9874783","GSM9874761","GSM9874777","GSM9874778","GSM9874775","GSM9874776","GSM9874759","GSM9874779","GSM9874770","GSM9874773","GSM9874774","GSM9874771","GSM9874772"],"GPL":["24676"],"GSE":["338460"],"taxon":["Homo sapiens"]}}