<HashMap><database>GEO</database><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</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=GSE331351</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Single-Cell Multi-Omics Reveals Activation of the STAT3–PIM1 Axis in T Cell Subsets in Proteinase 3-ANCA-Positive Granulomatosis with Polyangiitis</name><description>Granulomatosis with polyangiitis (GPA) is an autoimmune disease marked by relapses and treatment-related morbidity. CD4⁺ T cells play a central role in GPA pathogenesis, but their molecular profile remains incompletely defined. This study aimed to characterize CD4⁺ T cells in proteinase 3-ANCA-positive GPA (PR3-GPA) patients using single-cell multi-omics to identify molecular signatures associated with disease activity. Peripheral blood mononuclear cells were obtained from PR3-GPA patients during active disease, remission, and healthy controls. Single-cell RNA sequencing and CITE-seq were used to define transcriptional and protein expression profiles of CD4⁺ T cell subsets. Findings were validated using RT-qPCR, flow cytometry–based assays, including phospho-flow cytometry, and in vitro inhibition assay. scRNA-seq and CITE-seq revealed upregulated PIM1 expression in CD4⁺ T cell subsets in active GPA compared to controls. Pim kinase inhibition reduced CD4⁺ T cell activation, proliferation, and cytokine production. These findings indicate that circulating CD4⁺ T cells in active PR3-GPA are characterized by activation of the STAT3–PIM1 axis, potentially driven by upstream IL-6 signaling.</description><dates><publication>2026/05/25</publication></dates><accession>GSE331351</accession><cross_references><GSM>GSM9744493</GSM><GSM>GSM9744492</GSM><GSM>GSM9744494</GSM><GPL>24676</GPL><GSE>331351</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>