Lupus & antiphospholipid syndrome
Obesity-exacerbated lupus via leptin-induced putrescine depletion and Tfh cell hyperactivation
Authors' conclusion
Obesity-associated hyperleptinaemia could compound SLE via putrescine-implicated modulation of Tfh differentiation and concurrently contribute to a broad cytokine-driven inflammatory loop.
Study context
- Population
- Healthy controls and systemic lupus erythematosus (SLE) patients with active or remission state stratified by obesity
- Outcome
- Leptin levels
Methodological detailsmetabolomics/transcriptomic profiling, ODC1 silencing and putrescine (PUT) treatment in vitro
- Metabolomics/transcriptomic profiling
- ODC1 silencing and PUT treatment in vitro
Main finding
As reported in the abstract
- Significantly elevated in obese patients across all subgroups and correlated positively with autoantibodies
Further findings
Circulating Tfh (cTfh) and activated cTfh frequencies
- Increased in remission patients compared to controls; further elevated in obese patients and strongly correlated with leptin levels
Cytokines
- Multiple cytokines higher in SLE patients than healthy controls; obesity could exacerbate the cytokine dysregulation
Leptin-treated Jurkat cells (in vitro)
- Leptin upregulated PD-1 expression and altered genes related to polyamine metabolism, particularly ornithine
PUT levels
- Reduced in patients, especially with obesity
Bcl-6 and Blimp1 with PUT deficiency (in vitro)
- PUT deficiency increased Bcl-6 and decreased Blimp1, both reversible by PUT supplementation
Original publication
Obesity-exacerbated lupus via leptin-induced putrescine depletion and Tfh cell hyperactivation. Clin Exp Rheumatol. Published 23 January 2026. doi:10.
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