Systemic sclerosis & Raynaud's

IL-35 enhances IL-10⁺ breg-mediated immunoregulation and attenuates inflammation and fibrosis in systemic sclerosis

Arthritis Res TherPublished Mechanistic study

Authors' conclusion

While IL-35 is compensatorily elevated in SSc, its endogenous levels are insufficient to curb the disease.

Study context

Population
Treatment-naïve systemic sclerosis (SSc) patients and healthy controls; bleomycin-induced SSc mouse model
Participants
132 vs 58
Comparison
Treatment-naïve SSc patients vs healthy controls (HCs); IL-35 vs anti-IL-35 mAb
  • SScn = 132
  • HCsn = 58reference
Methodological detailscase-control comparison with HCs, in vitro B cell–T cell co-culture, bleomycin-induced SSc mouse model
  • Case-control comparison with HCs
  • In vitro B cell–T cell co-culture
  • Bleomycin-induced SSc mouse model

Main finding

As reported in the abstract

  • SSc: elevated plasma IL-35, IL-10, IL-6 and BAFF; increased CD19⁺ B cells and IL-6⁺ effector B cells
  • IL-35⁺ and IL-10⁺ Bregs significantly decreased in blood and skin
  • IL-10, IL-6 and TGF-β1 mRNA increased in skin lesions
  • IL-35 and IL-10 levels correlated with lung function, skin scores and inflammatory markers
  • In vitro, IL-35 promoted IL-10⁺ Breg expansion and cytokine secretion and suppressed Th1, Th17 and CD8⁺IFN-γ⁺ T cell responses via an IL-10-dependent mechanism
  • In vivo, IL-35 alleviated fibrosis and inflammation in bleomycin-treated mice; mAbIL-35 exacerbated it

Original publication

IL-35 enhances IL-10⁺ breg-mediated immunoregulation and attenuates inflammation and fibrosis in systemic sclerosis. Arthritis Res Ther. Published 30 January 2026. doi:10.1186/s13075-026-03735-8

Composed by AI from the published abstract and checked against it. How Briefs are made →

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