ReviewWorld journal of pediatrics : WJP2024
Type I interferon pathway in pediatric systemic lupus erythematosus.
Review in World journal of pediatrics : WJP, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- From metabolic disorder to autoimmunity: lupus-like immune dysregulation in children with SLC7A7-associated lysinuric protein intolerance.BMC pediatrics · 2026Review
- Real-world safety profile of anifrolumab: An observational disproportionality analysis of the FAERS database.Medicine · 2026Observational
- Immune ontogeny in childhood-onset systemic lupus erythematosus: effect of immune maturity on disease phenotype and therapeutic responses.Frontiers in immunology · 2026Review
- The Type I Interferon Axis in Systemic Autoimmune Diseases: From Molecular Pathways to Targeted Therapy.Biomolecules · 2025Review
- Toll-Like Receptors in the Immunotherapy Era: Dual-Edged Swords of Tumor Immunity and Clinical Translation.MedComm · 2025Review
- Innovative therapies for childhood-onset systemic lupus erythematosus.World journal of pediatrics : WJP · 2025Article
- Bioinformatic analysis and experimental verification reveal expansion of monocyte subsets with an interferon signature in systemic lupus erythematosus patients.Arthritis research & therapy · 2025Article
- ANGPTL3 in Podocytes Contributes to the Pathogenesis of Lupus Nephritis by Activating MSR1 in Macrophages.Kidney diseases (Basel, Switzerland)Article
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Authors and funding
2 authors.
Funding
Abstract
backgroundThe role of type I interferon (IFN-I) signaling in systemic lupus erythematosus (SLE) has been well established. However, unanswered questions remain regarding the applicability of these findings to pediatric-onset SLE. The aim of this review is to provide an overview of the novel discoveries on IFN-I signaling in pediatric-onset SLE. DATA SOURCES: A literature search was conducted in the PubMed database using the following keywords: "pediatric systemic lupus erythematosus" and "type I interferon".
resultsIFN-I signaling is increased in pediatric SLE, largely due to the presence of plasmacytoid dendritic cells and pathways such as cyclic GMP-AMP synthase-stimulator of interferon genes-TANK-binding kinase 1 and Toll-like receptor (TLR)4/TLR9. Neutrophil extracellular traps and oxidative DNA damage further stimulate IFN-I production. Genetic variants in IFN-I-related genes, such as IFN-regulatory factor 5 and tyrosine kinase 2, are linked to SLE susceptibility in pediatric patients. In addition, type I interferonopathies, characterized by sustained IFN-I activation, can mimic SLE symptoms and are thus important to distinguish. Studies on interferonopathies also contribute to exploring the pathogenesis of SLE. Measuring IFN-I activation is crucial for SLE diagnosis and stratification. Both IFN-stimulated gene expression and serum IFN-α2 levels are common indicators. Flow cytometry markers such as CD169 and galectin-9 are promising alternatives. Anti-IFN therapies, such as sifalimumab and anifrolumab, show promise in adult patients with SLE, but their efficacy in pediatric patients requires further investigation. Janus kinase inhibitors are another treatment option for severe pediatric SLE patients.
conclusionsThis review presents an overview of the IFN-I pathway in pediatric SLE. Understanding the intricate relationship between IFN-I and pediatric SLE may help to identify potential diagnostic markers and targeted therapies, paving the way for improved patient care and outcomes.
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