ArticleRheumatology (Oxford, England)2025
Targeting interferon responses in juvenile dermatomyositis: Siglec-1 as an in vitro biomarker for JAK inhibitor efficacy.
Article in Rheumatology (Oxford, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Towards New Strategies: Case Report and Review of the Literature-Effective Use of JAK Inhibitor Baricitinib in a 4-Year-Old Boy with Anti-MDA5 Antibody-Positive Juvenile Dermatomyositis.Journal of clinical medicine · 2026Article
- Role of myeloid cells expressing CD169/Siglec-1 in host-pathogen interactions.FEMS microbiology reviews · 2026Review
- Juvenile dermatomyositis: new insights into pathogenesis and clinical applications.Pediatric rheumatology online journal · 2025Review
- A fresh look at immunocytometry's role in personalized rheumatology.Rheumatology (Oxford, England) · 2025Article
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Authors and funding
19 authors.
Funding
Abstract
objectivesFor IFN-driven diseases, such as juvenile dermatomyositis (JDM), there is a critical need for targeted therapies. We aimed to develop an in vitro model, using Siglec-1 as read-out, to evaluate inhibition of IFN-mediated responses with different JAK inhibitors (JAKi).
methodsHealthy donor (HD) PBMCs were cultured with type I and II IFNs, TLR agonists and plasma or serum from patients (JDM, DM, JSLE, COVID-19) and HDs. Siglec-1 expression on CD14+ monocytes was analyzed using flow cytometry. Inhibitory assays involved pre-incubation with JAKi (filgotinib, tofacitinib, baricitinib, ruxolitinib, deucravacitinib) and interferon-α/β receptor (IFNAR)-blocking antibody. Correlations between plasma-induced Siglec-1 levels and clinical disease activity were analyzed in JDM patients, as well as correlations with IFN-α and -β plasma levels.
resultsSiglec-1 was induced after 18 h of stimulation with type I IFNs and TLR-3/7/9 agonists, with minimal induction by IFN-γ. IFNAR blockade prevented type I IFN- and TLR-mediated induction. JAKi inhibited Siglec-1 induction by IFN-α and -β in a dose-dependent manner. Co-culture with plasma or serum from patients with IFN-driven diseases induced Siglec-1 expression on healthy monocytes, which could be inhibited by JAKi and IFNAR blockade. Siglec-1 levels induced by JDM plasma correlated strongly with clinical disease activity and IFN-β plasma levels.
conclusionSiglec-1 is an easy and reliable in vitro marker for type I IFN responses. Its induction can be inhibited by JAKi. The type I IFN signature in JDM is likely predominantly driven by IFN-β. This assay holds promise for precision treatment strategies in JDM and other IFN-driven diseases.
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