ReviewCurrent opinion in rheumatology2019
Role of type I interferons and innate immunity in systemic sclerosis: unbalanced activities on distinct cell types?
Review in Current opinion in rheumatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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
11 citing papers in PubMed, 17 citations in OpenAlex.
- Tofacitinib blocks IFN-regulated biomarker genes in skin fibroblasts and keratinocytes in a systemic sclerosis trial.JCI insight · 2022Trial
- Tetrameric assembly disruption impairs CXCL4 chaperon ability for DNA and type I interferon immune amplification.Communications biology · 2026Article
- The Role of CXCL4 in Systemic Sclerosis: DAMP, Auto-Antigen and Biomarker.International journal of molecular sciences · 2025Review
- Sensing of SARS-CoV-2 by pDCs and their subsequent production of IFN-I contribute to macrophage-induced cytokine storm during COVID-19.Science immunology · 2022Article
- Article
- Review
- Targeting human plasmacytoid dendritic cells through BDCA2 prevents skin inflammation and fibrosis in a novel xenotransplant mouse model of scleroderma.Annals of the rheumatic diseases · 2021Article
- Noncytotoxic Inhibition of the Immunoproteasome Regulates Human Immune Cells In Vitro and Suppresses Cutaneous Inflammation in the Mouse.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Immune Cell-Stromal Circuitry in Lupus Photosensitivity.Journal of immunology (Baltimore, Md. : 1950) · 2021Review
- Novel insights into dendritic cells in the pathogenesis of systemic sclerosis.Clinical and experimental immunology · 2020Review
- Comparative Analysis of Inflammatory Response in Surgical Wound Drainage Fluid in Scoliosis Surgery: A Study of Neuromuscular vs. Idiopathic Patients.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
purpose of reviewThe role of type I IFNs (IFN-I) in the promotion of autoimmunity has been well established. However, its role in the skin fibrosis of systemic sclerosis (SSc) is less clear. IFN-I can participate to tissue repair, and, here, we will consider the extent to which IFN-I's role in SSc skin fibrosis may reflect in part IFN-I functions during wound healing. RECENT
findingsStudies are beginning to delineate whether IFN-I has a protective or pathogenic role and how IFN-I affects tissue biology. Recent support for a pathogenic role came from a study depleting plasmacytoid dendritic cells during bleomycin-induced skin fibrosis. The depletion reduced the bleomycin-induced IFN-I-stimulated transcripts and both prevented and reversed fibrosis. Additionally, two recent articles, one identifying SSc endothelial cell injury markers and one showing repressed IFN signaling in SSc keratinocytes, suggest the possibility of unbalanced IFN-I activities on distinct cells types. SUMMARY: Recent results support a pathogenic role for IFN-I in skin fibrosis, and recent studies along with others suggest a scenario whereby SSc skin damage results from too much IFN-I-activity driving vasculopathy in combination with too little IFN-I-mediated epidermal integrity and antifibrotic fibroblast phenotype.
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.