Lupus & antiphospholipid syndrome
Enhanced medullary and extramedullary granulopoiesis sustain the inflammatory response in lupus nephritis
Authors' conclusion
These data support a key role of granulocytes derived from primed HSPCs both at medullary and extramedullary sites in the pathogenesis of LN.
Study context
- Population
- Bone marrow (BM)-derived haematopoietic stem and progenitor cells (HSPCs) from patients with SLE and NZBW/F1 lupus-prone mice
Methodological detailstranscriptomic analysis, DNA methylation profile, NZBW/F1 lupus-prone mice, colony-forming unit assay, adoptive cell transfer
- Transcriptomic analysis
- DNA methylation profile
- NZBW/F1 lupus-prone mice
- Colony-forming unit assay
- Adoptive cell transfer
Main finding
As reported in the abstract
- Splenic HSPCs carry a higher inflammatory potential than BM HSPCs
- Induction of trained immunity with β-glucan exacerbates splenic extramedullary haematopoiesis, accentuates myeloid skewing and worsens lupus nephritis (LN)
- Methylomic analysis of BM-derived HSPCs shows myeloid skewing, in part driven by epigenetic tinkering
- Human SLE BM-derived HSPCs show transcriptomic findings similar to those in diseased mice
Original publication
Enhanced medullary and extramedullary granulopoiesis sustain the inflammatory response in lupus nephritis. Lupus Sci Med. Published 11 March 2024. doi:10.
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