ArticleArthritis research & therapy2018
Type I IFN signature in childhood-onset systemic lupus erythematosus: a conspiracy of DNA- and RNA-sensing receptors?
Article in Arthritis research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.
- Pooled it
- Pooled it
- Chimeric Antigen Receptor T-Cell Therapy in Autoimmune Disorders: An Expert Panel Opinion From the American Society for Transplantation and Cellular Therapy.Transplantation and cellular therapy · 2026Review
- Exploration of shared gene signatures and molecular mechanisms between psoriasis and COVID-19: evidence from transcriptome data.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- The landscape of cellular immune alteration in systemic lupus erythematosus.Frontiers in immunology · 2026Review
- Immune ontogeny in childhood-onset systemic lupus erythematosus: effect of immune maturity on disease phenotype and therapeutic responses.Frontiers in immunology · 2026Review
- The role of DNASE1L3 in systemic lupus erythematosus: from pathogenesis to clinical implications.Clinical and experimental medicine · 2025Review
- Type I interferon pathway in pediatric systemic lupus erythematosus.World journal of pediatrics : WJP · 2024Review
- IFN-I Score and Rare Genetic Variants in Children with Systemic Lupus Erythematosus.Biomedicines · 2024Article
- Cytosolic nucleic acid sensing and mitochondrial transcriptomic changes as early triggers of metabolic disease in db/db mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Article
- UnravelingFrontiers in oncology · 2024Review
- CAR T-cell therapy for systemic lupus erythematosus: current status and future perspectives.Frontiers in immunology · 2024Review
- Environment and systemic autoimmune rheumatic diseases: an overview and future directions.Frontiers in immunology · 2024Review
- A comprehensive analysis of type 1 interferon gene signatures in systematic lupus erythematosus and prediction of the crucial susceptible factor for Sjögren syndrome.Clinical and experimental medicine · 2023Article
- Potential relevance of type I interferon-related biomarkers for the management of polygenic autoimmune rheumatic diseases with childhood onset.Clinical rheumatology · 2023Article
- Genes and Microbiota Interaction in Monogenic Autoimmune Disorders.Biomedicines · 2023Review
- Review
- Integrative Bioinformatics Analysis Identifies DDX60 as a Potential Biomarker for Systemic Lupus Erythematosus.Disease markers · 2023Article
- Article
- A Study on MDA5 Signaling in Splenic B Cells from an Imiquimod-Induced Lupus Mouse Model with Proteomics.Cells · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundChildhood-onset systemic lupus erythematosus (cSLE) is an incurable multi-systemic autoimmune disease. Interferon type I (IFN-I) plays a pivotal role in the pathogenesis of SLE. The objective of this study was to assess the prevalence of the IFN-I signature and the contribution of cytosolic nucleic acid receptors to IFN-I activation in a cohort of primarily white cSLE patients.
methodsThe IFN-I score (positive or negative), as a measure of IFN-I activation, was assessed using real-time quantitative PCR (RT-PCR) expression values of IFN-I signature genes (IFI44, IFI44L, IFIT1, Ly6e, MxA, IFITM1) in CD14+ monocytes of cSLE patients and healthy controls (HCs). Innate immune receptor expression was determined by RT-PCR and flow cytometry. To clarify the contribution of RNA-binding RIG-like receptors (RLRs) and DNA-binding receptors (DBRs) to IFN-I activation, peripheral blood mononuclear cells (PBMCs) from patients were treated with BX795, a TANK-binding kinase 1 (TBK1) inhibitor blocking RLR and DBR pathways.
resultsThe IFN-I signature was positive in 57% of cSLE patients and 15% of the HCs. Upregulated gene expression of TLR7, RLRs (IFIH1, DDX58, DDX60, DHX58) and DBRs (ZBP-1, IFI16) was observed in CD14+ monocytes of the IFN-I-positive cSLE patients. Additionally, RIG-I and ZBP-1 protein expression was upregulated in these cells. Spontaneous IFN-I stimulated gene (ISG) expression in PBMCs from cSLE patients was inhibited by a TBK1-blocker.
conclusionsIFN-I activation, assessed as ISG expression, in cSLE is associated with increased expression of TLR7, and RNA and DNA binding receptors, and these receptors contribute to IFN-I activation via TBK1 signaling. TBK1-blockers may therefore be a promising treatment target for SLE.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.