Lupus & antiphospholipid syndrome
Bioinformatic analysis and experimental verification reveal expansion of monocyte subsets with an interferon signature in systemic lupus erythematosus patients
Authors' conclusion
Our study found that the expansion of IFN-I-producing monocyte subsets, particularly the CD14+SIGLEC1+IRF7+ subset, plays a crucial role in SLE pathogenesis.
Study context
- Population
- Transcriptome data from peripheral blood mononuclear cells (PBMCs) and monocytes of systemic lupus erythematosus (SLE) patients and healthy controls
- Comparison
- SLE patients vs healthy controls
Methodological detailsbioinformatic analysis (robust rank aggregation (RRA), DESeq2, limma), Single-cell RNA sequencing (scRNA-seq) (Seurat), flow cytometry validation
- Bioinformatic analysis (RRA, DESeq2, limma)
- scRNA-seq (Seurat)
- Flow cytometry validation
Main finding
As reported in the abstract
- Monocytes in SLE undergo IFN-driven transcriptional reprogramming with upregulation of key interferon signature genes (ISGs) (SLERRAsignature)
- Increase trend in proportion of CD14Mono8 subset in the flare group
- Differentially expressed genes (DEGs) in 13 mononuclear phagocyte subsets of SLE are mainly ISGs; ISG expression higher in severe patients
- SIGLEC1+IRF7+ monocytes identified, also found in peripheral blood of healthy individuals
- Enrichment score of SIGLEC1+IRF7+ monocyte gene set positively correlated with SLE severity
- Frequency of CD14+SIGLEC1+IRF7+ monocytes in PBMCs higher in SLE vs healthy controls (flow cytometry)
Original publication
Bioinformatic analysis and experimental verification reveal expansion of monocyte subsets with an interferon signature in systemic lupus erythematosus patients. Arthritis Res Ther. Published 25 April 2025. doi:10.
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