Lupus & antiphospholipid syndrome
Single-cell profiling reveals kidney CD163+ dendritic cell participation in human lupus nephritis
Authors' conclusion
The intricate interplay involving DC3s, T cells and tubular epithelial cells within kidneys may substantially contribute to LN pathogenesis.
Study context
- Population
- Patients with LN undergoing renal biopsy and healthy donors; matched peripheral blood from 7 LN patients; independent cohort of 60 patientsindependent cohort of 60 patients
- Participants
- 40 vs 6
- Comparison
- LN kidneys vs healthy donor kidneys
- LNn = 40
- Healthy donorsn = 6reference
Methodological detailssingle-cell RNA and T cell receptor sequencing, multiplex immunohistochemistry, flow cytometry, in vitro assays, independent validation cohort
- Single-cell RNA and T cell receptor sequencing
- Multiplex immunohistochemistry
- Flow cytometry
- In vitro assays
- Independent validation cohort
Main finding
As reported in the abstract
- Notable enrichment of CD163+ dendritic cells (DC3s) in LN kidneys, positively correlated with LN severity
- Kidney DC3s in LN displayed activated, highly proinflammatory phenotype vs blood counterparts
- DC3s interacted strongly with CD4+ T cells, contributing to intrarenal T cell clonal expansion, CD4+ effector T cell activation and Th1/Th17 polarisation
- Injured proximal tubular epithelial cells (iPTECs) may orchestrate DC3 activation, adhesion and recruitment in LN kidneys
- In culture, blood DC3s treated with iPTECs acquired distinct capabilities to polarise Th1/Th17 cells
- Kidney DC3 enumeration might be a potential biomarker for induction treatment response in LN
Original publication
Single-cell profiling reveals kidney CD163+ dendritic cell participation in human lupus nephritis. Ann Rheum Dis. Published 11 April 2024. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →