ArticleScientific reports2017
Transcriptional dysregulation of Interferome in experimental and human Multiple Sclerosis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Impact of machine learning-driven analysis of blood transcriptomes in multiple sclerosis.Neural regeneration research · 2026Article
- Robust CD4medRxiv : the preprint server for health sciences · 2025Article
- A disease-specific convergence of host and Epstein-Barr virus genetics in multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Central TYK2 inhibition identifies TYK2 as a key neuroimmune modulator.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- In Silico Analysis Highlights Potential Predictive Indicators Associated with Secondary Progressive Multiple Sclerosis.International journal of molecular sciences · 2024Article
- Circulating MAIT cells in multiple sclerosis and amyotrophic lateral sclerosis.Frontiers in immunology · 2024Article
- AnMolecular genetics and metabolism reports · 2023Article
- The value of Interferon β in multiple sclerosis and novel opportunities for its anti-viral activity: a narrative literature review.Frontiers in immunology · 2023Review
- Gene expression signatures of target tissues in type 1 diabetes, lupus erythematosus, multiple sclerosis, and rheumatoid arthritis.Science advances · 2021Article
- Differential modulation of Ahr and Arid5a: A promising therapeutic strategy for autoimmune encephalomyelitis.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020Article
- Inferring Multiple Sclerosis Stages from the Blood Transcriptome via Machine Learning.Cell reports. Medicine · 2020Article
- RETRACTED ARTICLE: Selected TLR7/8 agonist and type I interferon (IFN-α) cooperatively redefine the microglia transcriptome.Inflammopharmacology · 2020Article
- Loss of Circulating CD8+ CD161Frontiers in immunology · 2019Article
- CHP1 reduction ameliorates spinal muscular atrophy pathology by restoring calcineurin activity and endocytosis.Brain : a journal of neurology · 2018Article
- An Integrated Bioinformatics Analysis of the Potential Regulatory Effects of miR-21 on T-cell Related Target Genes in Multiple Sclerosis.Avicenna journal of medical biotechnologyArticle
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence indicates that single multiple sclerosis (MS) susceptibility genes involved in interferon (IFN) signaling display altered transcript levels in peripheral blood of untreated MS subjects, suggesting that responsiveness to endogenous IFN is dysregulated during neuroinflammation. To prove this hypothesis we exploited the systematic collection of IFN regulated genes (IRG) provided by the Interferome database and mapped Interferome changes in experimental and human MS. Indeed, central nervous system tissue and encephalitogenic CD4 T cells during experimental autoimmune encephalomyelitis were characterized by massive changes in Interferome transcription. Further, the analysis of almost 500 human blood transcriptomes showed that (i) several IRG changed expression at distinct MS stages with a core of 21 transcripts concordantly dysregulated in all MS forms compared with healthy subjects; (ii) 100 differentially expressed IRG were validated in independent case-control cohorts; and (iii) 53 out of 100 dysregulated IRG were targeted by IFN-beta treatment in vivo. Finally, ex vivo and in vitro experiments established that IFN-beta administration modulated expression of two IRG, ARRB1 and CHP1, in immune cells. Our study confirms the impairment of Interferome in experimental and human MS, and describes IRG signatures at distinct disease stages which can represent novel therapeutic targets in MS.
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