Lupus & antiphospholipid syndrome
IL-2 signalling sustains pathogenic age-associated B cell homeostasis in lupus
Authors' conclusion
This study identified ABCs as a novel target of IL-2, expanding the understanding of IL-2's role in SLE beyond the traditional Treg-centric view and offering insights into the variable therapeutic efficacy of IL-2 in this context.
Study context
- Population
- ABCs in systemic lupus erythematosus (SLE): transcriptomic data, TLR7-driven lupus-prone mice and patients with SLE
- Outcome
- Effects of IL-2 signalling on ABCs
Methodological detailsintegrated transcriptomic and single-cell analyses, TLR7-driven lupus-prone mice, adoptive transfer, bioinformatic analysis of patients with SLE
- Integrated transcriptomic and single-cell analyses
- TLR7-driven lupus-prone mice
- Adoptive transfer
- Bioinformatic analysis of patients with SLE
Main finding
As reported in the abstract
- Elevated IL-2 signalling in ABCs, more pronounced IL-2 signature in SLE than in healthy controls
- IL2RB significantly enriched in ABCs, with increased chromatin accessibility at its promoter
- IL-2 promoted ABC survival and differentiation in a stage-dependent manner
- Prior IL-2 administration to recipient mice promoted persistence of adoptively transferred ABCs
- In lupus-prone mice, IL-2 increased both ABC and Treg populations without ameliorating disease manifestations; ABC promotion more dependent on disease condition
- ABCs showed elevated IL-2 receptor expression correlating with ABC frequency; IL-2 signalling activation in B cells and ABCs from patients with SLE
Original publication
IL-2 signalling sustains pathogenic age-associated B cell homeostasis in lupus. Ann Rheum Dis. Published 11 September 2025. doi:10.
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