Lupus & antiphospholipid syndrome

Kidney whole-transcriptome profiling in primary antiphospholipid syndrome reveals complement, interferons and neutrophil-extracellular traps (NETs)-related gene expression

Rheumatology (Oxford)Published Mechanistic study

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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