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Updated: Mar 16, 2026

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
Published on: June 15, 2016
Single-cell transcriptomics identifies NF-κB/STAT3-associated neutrophil inflammatory reprogramming in rheumatoid
Jianbin Li1, Pengcheng Liu1, Jun Zhao1
1Department of Rheumatology and Immunology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
None:
To elucidate neutrophil heterogeneity in rheumatoid arthritis (RA) synovium, we performed single-cell RNA sequencing on 8 RA patients (66,539 cells), stratified by neutrophil infiltration status. Infiltrating neutrophils predominantly displayed inflammatory C1 (Chemokine+) and C3 (S100A8/A9+) phenotypes. Co-expression analysis (hdWGCNA) identified two functional modules (M3/M4) enriched in NF-κB and type I interferon signaling. Furthermore, these neutrophils actively reshaped the synovial microenvironment via CXCL, IL1, and MIF communication pathways. Transcriptional inference and comparative in silico knockouts revealed the NF-κB/STAT3 axis as a candidate regulatory node, with NFKB1 uniquely perturbing S100A8/A9 effector genes. Key findings, including M4 module activation and its correlation with systemic inflammatory markers (ESR/CRP), were validated in an independent bulk RNA-seq cohort (n = 19). This study comprehensively characterizes RA neutrophil inflammatory reprogramming and nominates the NF-κB/STAT3 axis for future functional validation.
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