Lupus & antiphospholipid syndrome
Kidney whole-transcriptome profiling in primary antiphospholipid syndrome reveals complement, interferons and neutrophil-extracellular traps (NETs)-related gene expression
Authors' conclusion
Complement, interferon and NETs-related genes are highly expressed in APS kidney tissues, similarly to SLE, pointing out the role of innate immunity in APS nephropathy pathogenesis and potential treatment targets.
Study context
- Population
- Individuals with primary antiphospholipid syndrome (APS), systemic lupus erythematosus (SLE) and controls with archival kidney biopsies
- Participants
- 4 / 5 / 3
- Comparison
- Primary APS vs SLE and control kidney biopsies
- APSn = 4
- SLEn = 5
- Controln = 3reference
- Outcome
- Kidney transcriptome profiles
Methodological detailsRNA sequencing of archival formalin-fixed paraffin-embedded kidney biopsies, differential gene expression analysis, enrichment analysis (gene ontology (GO), CORUM, KEGG, Reactome)
- RNA sequencing of archival formalin-fixed paraffin-embedded kidney biopsies
- Differential gene expression analysis
- Enrichment analysis (GO, CORUM, KEGG, Reactome)
Main finding
As reported in the abstract
Kidney transcriptome, APS vs controls and vs SLE
LogFC C3
2.25
P = 1.58e-05
APS
LogFC C4A
2.17
P = 2.69e-06
APS
LogFC C4B
2.135
P = 3.7e-06
APS
- Upregulated genes, APS vs controls
- 276
- Downregulated genes, APS vs controls
- 217
- Upregulated genes, APS vs SLE
- 75
- Downregulated genes, APS vs SLE
- 111
- Interferon (IFN) alpha/beta signalling revealed by Reactome; IFN-regulated genes upregulated in APS vs controls (P-values ≤ 0.001 for all)
- 9
- NETs-related genes with higher expression in APS vs controls but not vs SLE (of 15 upregulated)
- 13
Original publication
Kidney whole-transcriptome profiling in primary antiphospholipid syndrome reveals complement, interferons and NETs-related gene expression. Rheumatology (Oxford). Published 6 August 2024. doi:10. 1093/ rheumatology/ keae397
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