Lupus & antiphospholipid syndrome
Podocyte Interleukin‐23 Receptor Signaling in the Pathogenesis of Lupus Nephritis
Authors' conclusion
IL-23R expression is increased in podocytes from mice and humans with systemic lupus erythematosus. IL-23 signaling disrupts the cytoskeleton in podocytes and increases their mobility, leading to the development of glomerulonephritis. Podocyte-specific deletion of Il23r in lupus-prone mice abrogates the development of LN.
Study context
- Population
- Kidney biopsies of patients with lupus nephritis (LN); human podocyte cell line, primary murine podocytes; B6 wild-type mice injected with IL-23 minicircle (MC); MRL/lpr mice
- Comparison
- Podocyte-specific Il23r deletion vs intact IL-23R in lupus-prone MRL/lpr mice; IL-23 stimulation of podocytes
Methodological detailshuman kidney biopsies, in vitro human and murine podocytes, bulk RNA sequencing, podocyte-specific Il23r-deficient MRL/lpr mice
- Human kidney biopsies
- In vitro human and murine podocytes
- Bulk RNA sequencing
- Podocyte-specific Il23r-deficient MRL/lpr mice
Main finding
As reported in the abstract
- IL-23R highly expressed in glomeruli of patients with LN
- IL-23R expression up-regulated in human podocytes and primary podocytes from B6 mice after IL-23 stimulation
- IL-23-stimulated human podocytes: decreased synaptopodin expression and actin cytoskeleton remodeling
- IL-23 MC mice: significant increase in IL-23R and phosphorylated STAT3 in podocytes
- MRL/lpr.Podo-Cre+ Il23rfl/fl mice: decreased clinical and histologic features of LN
Original publication
Podocyte Interleukin‐23 Receptor Signaling in the Pathogenesis of Lupus Nephritis. Arthritis Rheumatol. Published 30 December 2025. doi:10.
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