Lupus & antiphospholipid syndrome

Interleukin‐12 Signaling Promotes Podocyte Senescence in Lupus Nephritis

Arthritis RheumatolPublished Mechanistic study

Authors' conclusion

Our findings identify IL-12 signaling as an important mediator of podocyte senescence in LN

Study context

Population
Patients with SLE (including lupus nephritis (LN)) and healthy controls; lupus-prone and nephrotoxic nephritis mouse models
Participants
39 / 15 / 13
Comparison
Podocyte-specific Il12rb1 knockout mice vs B6.Il12rb1fl/fl and B6.lpr.Il12rb1fl/fl controls; patients with SLE/LN vs healthy controls
  • SLEn = 39
  • LNn = 15
  • Healthy controlsn = 13reference
Outcome
IL-12 signalling and podocyte senescence in LN (serum IL-12, podocyte IL-12R expression, effects of IL-12 and of podocyte-specific Il12rb1 deletion)
Methodological detailshuman sera and kidney tissue, immortalized human podocyte cell line in vitro, podocyte conditional Il12rb1 knockout mice, accelerated lupus model and nephrotoxic nephritis model
  • Human sera and kidney tissue
  • Immortalized human podocyte cell line in vitro
  • Podocyte conditional Il12rb1 knockout mice
  • Accelerated lupus model and nephrotoxic nephritis model

Main finding

As reported in the abstract

Serum IL-12 elevated in patients with LN
P = 0.006
Serum IL-12 elevated in lupus-prone mice
P = 0.041

Original publication

Interleukin‐12 Signaling Promotes Podocyte Senescence in Lupus Nephritis. Arthritis Rheumatol. Published 24 August 2026. doi:10.1002/art.70305

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