Lupus & antiphospholipid syndrome
Disease activity drives divergent epigenetic and transcriptomic reprogramming of monocyte subpopulations in systemic lupus erythematosus
Authors' conclusion
Disease activity in SLE drives a subversion of the epigenome and transcriptome programme in monocyte differentiation, impacting the function of different subsets and allowing to generate predictive methods for activity and progression.
Study context
- Population
- Classic, intermediate and non-classic monocytes from patients with systemic lupus erythematosus (SLE) and healthy donors
- Comparison
- Patients with SLE vs healthy donors
- Outcome
- Epigenetic and transcriptomic profiles of monocyte subsets
Methodological detailsDNA methylomes and transcriptomes of monocyte subsets, integration with single-cell transcriptomics, first and follow-up visits
- DNA methylomes and transcriptomes of monocyte subsets
- Integration with single-cell transcriptomics
- First and follow-up visits
Main finding
As reported in the abstract
- Shared DNA methylation and transcriptomic alterations associated with a strong interferon signature
- Monocyte subset-specific alterations, especially in DNA methylation, reflecting an impact of SLE on monocyte differentiation
- SLE classic monocytes: proinflammatory profile, primed for macrophage differentiation
- SLE non-classic monocytes: T cell differentiation-related phenotype with Th17-regulating features
- Changes in monocyte proportions, DNA methylation and expression related to disease activity, involving the STAT pathway
- Single-cell integration: disease activity-dependent expansion of SLE-specific monocyte subsets; interferon signature in classic monocytes; intermediate and non-classic populations associated with exacerbated complement activation
Original publication
Disease activity drives divergent epigenetic and transcriptomic reprogramming of monocyte subpopulations in systemic lupus erythematosus. Ann Rheum Dis. Published 12 June 2024. doi:10.
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