ArticleBlood2016
Type I interferon causes thrombotic microangiopathy by a dose-dependent toxic effect on the microvasculature.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.
What it found
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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
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.
- The cytokines interleukin-6 and interferon-α induce distinct microglia phenotypes.Journal of neuroinflammation · 2022Pooled it
- Multisystem inflammation and susceptibility to viral infections in human ZNFX1 deficiency.The Journal of allergy and clinical immunology · 2021Trial
- Endothelial injury is a central driver of systemic IFN-β toxicity and is reversible through Jak inhibition.Molecular therapy. Oncology · 2026Article
- Avidity of autoantibodies against type I interferons as a factor associated with neurological complications in severe COVID-19.Frontiers in immunology · 2026Article
- Beta Interferon 1a and Laquinimod Differentially Affect Coagulation-Related Gene Expression in Multiple Sclerosis Patients: Implications for Clinical Efficacy and Side Effects.International journal of molecular sciences · 2025Article
- Article
- Post-transplant Thrombotic Microangiopathy.Journal of the American Society of Nephrology : JASN · 2025Review
- Article
- Risk of cardiovascular and autoimmune disease in people with multiple sclerosis on long-term interferon-β therapy.Brain communications · 2025Article
- Non-neutralizing anti-type I interferon autoantibodies could increase thrombotic risk in critical COVID-19 patients.Frontiers in immunology · 2025Article
- Pharmacological evaluation of drug therapies in Aicardi-Goutières syndrome: insights from patient-derived neural stem cells.Frontiers in pharmacology · 2025Article
- The prototypical interferonopathy: Aicardi-Goutières syndrome from bedside to bench.Immunological reviews · 2024Review
- Engineered CD4 T cells for in vivo delivery of therapeutic proteins.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The brain microvasculature is a primary mediator of interferon-α neurotoxicity in human cerebral interferonopathies.Immunity · 2024Article
- IL-6-mediated endothelial injury impairs antiviral humoral immunity after bone marrow transplantation.The Journal of clinical investigation · 2024Article
- Interferons prime the endothelium for toll-like receptor-mediated thrombin generation.Journal of thrombosis and haemostasis : JTH · 2024Article
- Thrombotic Microangiopathy as a Life-Threatening Complication of Long-Term Interferon Beta Therapy for Multiple Sclerosis: Clinical Phenotype and Response to Treatment-A Literature Review.Journal of clinical medicine · 2024Review
- TAFRO syndrome is associated with anti-SSA/Ro60 antibodies, in contrast to idiopathic castleman disease.Scientific reports · 2024Article
- Interferon-α receptor antisense oligonucleotides reduce neuroinflammation and neuropathology in a mouse model of cerebral interferonopathy.The Journal of clinical investigation · 2024Article
- PSMC3 proteasome subunit variants are associated with neurodevelopmental delay and type I interferon production.Science translational medicine · 2023Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 15 institutions in 5 countries.
Funding
Abstract
Many drugs have been reported to cause thrombotic microangiopathy (TMA), yet evidence supporting a direct association is often weak. In particular, TMA has been reported in association with recombinant type I interferon (IFN) therapies, with recent concern regarding the use of IFN in multiple sclerosis patients. However, a causal association has yet to be demonstrated. Here, we adopt a combined clinical and experimental approach to provide evidence of such an association between type I IFN and TMA. We show that the clinical phenotype of cases referred to a national center is uniformly consistent with a direct dose-dependent drug-induced TMA. We then show that dose-dependent microvascular disease is seen in a transgenic mouse model of IFN toxicity. This includes specific microvascular pathological changes seen in patient biopsies and is dependent on transcriptional activation of the IFN response through the type I interferon α/β receptor (IFNAR). Together our clinical and experimental findings provide evidence of a causal link between type I IFN and TMA. As such, recombinant type I IFN therapies should be stopped at the earliest stage in patients who develop this complication, with implications for risk mitigation.
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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.