Lupus & antiphospholipid syndrome
Inhibition of stimulator of interferon genes (STING) modulates dendritic cell responses and ameliorates podocyte injury in SLE
Authors' conclusion
Our findings suggest a potential role for STING in the interplay between immune dysregulation and podocyte injury in lupus.
Study context
- Population
- Patients with SLE, healthy controls, patients with lupus nephritis (LN) (kidney biopsies) and MRL/lpr mice
- Participants
- 28 / 15 / 39
- Comparison
- SLE vs healthy controls; STING inhibitor C176 in MRL/lpr mice
- SLEn = 28
- Healthy controlsn = 15reference
- LNn = 39
Methodological detailshuman peripheral blood mononuclear cells (PBMCs) and kidney biopsies, MRL/lpr mouse model, in vivo and in vitro
- Human PBMCs and kidney biopsies
- MRL/lpr mouse model
- In vivo and in vitro
Main finding
As reported in the abstract
- STING expression significantly elevated in PBMCs from patients with SLE and kidney tissues from patients with LN, particularly proliferative LN
- Renal STING correlated with glomerular proliferation and decreased synaptopodin expression
- STING activation promoted dendritic cell (DC) activation and plasmacytoid DC (pDC) differentiation
- Conditioned media from STING-activated DCs induced podocyte apoptosis and reduced synaptopodin, attenuated by STING inhibition
- C176 in MRL/lpr mice significantly alleviated splenomegaly, proteinuria, kidney inflammation and renal dysfunction, restoring podocyte integrity and reshaping immune responses
Original publication
Inhibition of STING modulates dendritic cell responses and ameliorates podocyte injury in SLE. Lupus Sci Med. Published 23 September 2026. doi:10.
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