Evidence map›Paper›PMID 40590520›Full record

ArticleInternational journal of rheumatic diseases2025

Patients With IgA Vasculitis and Kawasaki Disease Show Dysregulated Interferon Signature.

Sevki Erdem Varol, Cisem Cinar, Nihan Burtecene, Sezgin Sahin, Mehmet Yildiz, Kenan Barut, Haluk Cokugras, Sinem Firtina, Ozgur Kasapcopur, Ayca Kiykim

Abstract read
In one paragraph

Article in International journal of rheumatic diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Sevki Erdem VarolDepartment of Pediatrics, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Türkiye.
Cisem CinarDepartment of Medical Genetics, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Türkiye.
Nihan BurteceneDepartment of Pediatric Immunology and Allergy, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Türkiye.
Sezgin SahinDepartment of Pediatric Rheumatology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Türkiye.
Mehmet YildizDepartment of Pediatric Rheumatology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Türkiye.
Kenan BarutDepartment of Pediatric Rheumatology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Türkiye.
Haluk CokugrasDepartment of Pediatric Immunology and Allergy, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Türkiye.
Sinem FirtinaDepartment of Medical Genetics, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Türkiye.
Ozgur KasapcopurDepartment of Pediatric Rheumatology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Türkiye.ORCID https://orcid.org/0000-0002-1125-7720
Ayca KiykimDepartment of Pediatric Immunology and Allergy, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Türkiye.ORCID https://orcid.org/0000-0001-5821-3963

Funding

Scientific Research Projects Coordination Unit of Istanbul University-Cerrahpasa TTU-2023-37266Turkish Pediatric Society Decision no. 8 September 2023/11
6 · The paper itself

Abstract

objectiveIgA vasculitis (IgAV) and Kawasaki disease (KD) are the most common forms of childhood vasculitis. Although various factors such as viral infections, genetic factors, and environmental factors are involved in the development of both diseases, their pathogenesis remains unclear. The interferon (IFN) signature, which reflects the activation of type I IFN signaling pathways, is a diagnostic and prognostic tool that contributes significantly to the pathogenesis and management of autoimmune diseases. In our study, we aimed to investigate the role of the IFN signature in patients with IgAV and KD. MATERIAL AND

methodsThirty-two children with IgAV and four patients diagnosed with KD were included in the study. Serum levels of IL-1, IL-6, IL-8, IL-10, IL-17, IL-18, TNF-α, TNF-R1, TNF-R2, and IFN-gamma were analyzed in the serum samples of all participants, and the expression of IFN-related genes (STAT1, IFI27, IFI44, IFI44L, IFIT1, and RSAD2) was assessed in the patients and healthy controls (n = 26) to calculate the IFN score by RT-PCR method.

resultsA significant increase in the expression of three genes (IFIT1, IFI44, and IFI27) and decreased expression of the other three genes (RSAD2, STAT1, and IFI44L) was found in patients with IgAV and KD compared to the control group. Significantly higher IFN scores (IFN > 3) were found in patients with gastrointestinal involvement, in patients who required corticosteroid therapy, and in patients who had to be hospitalized. No significant difference in IFN levels was found between patients with and without renal involvement. Significantly higher serum IL-1 levels were found in patients with gastrointestinal symptoms with IgAV. High IFN scores were found in three out of four patients diagnosed with KD.

conclusionA dysregulated type 1 IFN signature was found in patients with IgAV and KD compared to the control group. A significantly increased risk of gastrointestinal involvement required corticosteroid therapy, and hospitalization was observed in patients diagnosed with IgAV who had high IFN levels. This underlines the idea that the IFN score could serve as a crucial prognostic indicator.

Indexed as

IgA VasculitisImmunoglobulin AInterferonsInterferon Type IMucocutaneous Lymph Node SyndromeAdaptor Proteins, Signal TransducingAntigensBiomarkersCarrier ProteinsCase-Control StudiesChildChild, PreschoolCytoskeletal ProteinsFemaleHumansInfantAdaptor Proteins, Signal TransducingAntigensBiomarkersCarrier ProteinsCytoskeletal ProteinsIFI27 protein, humanIFI44L protein, humanIFI44 protein, humanImmunoglobulin AInterferonsInterferon Type IMembrane ProteinsSTAT1 protein, humanSTAT1 Transcription FactorTumor Suppressor Proteinschildrenimmunoglobulin A vasculitisinterferon signatureKawasaki disease

Identifiers

PMID40590520
PMCPMC12211545

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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.