ArticleFrontiers in immunology2022
Assessment of type I interferon signatures in undifferentiated inflammatory diseases: A Japanese multicenter experience.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 25 citations in OpenAlex.
- Molecular mechanisms in rare proteasomopathies.EULAR rheumatology open · 2026Review
- Myeloperoxidase-positive mononuclear cells predominate over CD3-positive T-lymphocytes in the epidermis of Stevens-Johnson syndrome and toxic epidermal necrolysis.Virchows Archiv : an international journal of pathology · 2025Article
- Novel Compound Heterozygous Mutations in HOIP Result in Autoinflammation and Immunodeficiency.Journal of clinical immunology · 2025Article
- Understanding neurodevelopmental proteasomopathies as new rare disease entities: A review of current concepts, molecular biomarkers, and perspectives.Genes & diseases · 2024Review
- Proteasome-Associated Syndromes: Updates on Genetics, Clinical Manifestations, Pathogenesis, and Treatment.Journal of clinical immunology · 2024Review
- Safety and efficacy of canakinumab treatment for undifferentiated autoinflammatory diseases: the data of a retrospective cohort two-centered study.Frontiers in medicine · 2023Article
- A prognostic mathematical model based on tumor microenvironment-related genes expression for breast cancer patients.Frontiers in oncology · 2023Article
- Metabolic signature and proteasome activity controls synovial migration ofFrontiers in immunology · 2023Article
- Rituximab in Idiopathic Pulmonary Hemosiderosis in Children: A Novel and Less Toxic Treatment Option.Pharmaceuticals (Basel, Switzerland) · 2022Article
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Authors and funding
46 authors at 20 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Upregulation of type I interferon (IFN) signaling has been increasingly detected in inflammatory diseases. Recently, upregulation of the IFN signature has been suggested as a potential biomarker of IFN-driven inflammatory diseases. Yet, it remains unclear to what extent type I IFN is involved in the pathogenesis of undifferentiated inflammatory diseases. This study aimed to quantify the type I IFN signature in clinically undiagnosed patients and assess clinical characteristics in those with a high IFN signature. Methods: The type I IFN signature was measured in patients' whole blood cells. Clinical and biological data were collected retrospectively, and an intensive genetic analysis was performed in undiagnosed patients with a high IFN signature. Results: A total of 117 samples from 94 patients with inflammatory diseases, including 37 undiagnosed cases, were analyzed. Increased IFN signaling was observed in 19 undiagnosed patients, with 10 exhibiting clinical features commonly found in type I interferonopathies. Skin manifestations, observed in eight patients, were macroscopically and histologically similar to those found in proteasome-associated autoinflammatory syndrome. Genetic analysis identified novel mutations in the Conclusions: Half of the patients examined in this study, with undifferentiated inflammatory diseases, clinically quiescent A20 haploinsufficiency, or idiopathic pulmonary hemosiderosis, had an elevated type I IFN signature.
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