GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE328nnn/GSE328518/primaryOK200GenomicsHomo sapiensNon-coding RNA profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328518GEOGSEfalseCD4+ T Cell-Derived Exosomal miR-223-3p Serves as a Potential Biomarker for Systemic Lupus Erythematosus and Attenuates Lupus Nephritis in NZBWF1/J MiceThis study aimed to identify key exosomal miRNAs derived from CD4+ T cells in SLE and assess their potential for diagnosis and therapy. The results showed that CD4+ T cell-derived exosomal miR-223-3p was downregulated in SLE patients and demonstrated modest diagnostic performance (AUC = 0.71, 95% CI: 0.65–0.77). When combined with conventional clinical markers, it provided incremental diagnostic value. Its correlation with clinical markers (Anti-Sm, C3/C4) was specific to the CD4+ T cell-derived exosomal fraction, distinguishing it from the plasma-derived counterpart. Functionally, miR-223-3p overexpression inhibited the secretion of inflammatory cytokines and the apoptosis of T cells, while promoting mitophagy through FBXW7. Additionally, it disrupted pathological T-B cell interactions by suppressing BAFF and CD19 expression. In a murine lupus model (NZBWF1/J), administration of exosomal miR-223-3p alleviated lupus nephritis, as evidenced by reduced proteinuria, lower anti-dsDNA titers, and diminished renal immune complex deposition. Collectively, this study identified CD4+ T cell-derived exosomal miR-223-3p as a cell origin-associated biomarker in SLE, while also acting as a pathogenic regulator through the FBXW7/mitophagy axis and modulation of T-B cell crosstalk. Its therapeutic efficacy in vivo supports its potential as a candidate for exosome-based therapy in SLE.2026/09/30GSE328518GSM9684702GSM9684701GSM9684700GSM9684699GSM9684698GSM9684697GSM9684704GSM968470324676328518Homo sapiens[42381062]