ArticleImmunity2022
Excessive negative regulation of type I interferon disrupts viral control in individuals with Down syndrome.
Article in Immunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Revisiting down syndrome through the lens of interferonopathy and innate immune dysregulation.Frontiers in immunology · 2026Pooled it
- Polymorphism in interferon alpha/beta receptor contributes to glucocorticoid response and outcome of ARDS and COVID-19.Critical care (London, England) · 2023Trial
- T-cell responses to primary SARS-CoV-2 vaccination in Down syndrome - From childhood to adulthood.Human vaccines & immunotherapeutics · 2026Observational
- Clinical considerations for immune dysregulation and immunodeficiency in Down syndrome.Journal of human immunity · 2026Review
- Immune Dysregulation in Down Syndrome: Implications for Infectious Susceptibility and Vaccine Response.Journal of clinical immunology · 2026Review
- Endocrine and Digestive Disorders Arising in Childhood in Down Syndrome and Their Cross-Talk.Nutrients · 2026Review
- Down Syndrome Alters Type III IFN and Proinflammatory Airway Epithelial Responses to Respiratory Syncytial Virus Infection.American journal of respiratory cell and molecular biology · 2025Article
- Clinical and Immunological Impact of JAK Inhibition in Concurrent Down Syndrome and STAT1 Gain of Function.Journal of clinical immunology · 2025Article
- Perspectives on the origin and therapeutic opportunities in Down syndrome-associated leukemia.Cancer metastasis reviews · 2025Review
- Rheumatologic and Autoimmune Features of Inborn Errors of Immunity: Implications for Diagnosis and Management.Journal of human immunity · 2025Article
- Interferons in health and disease.Cell · 2025Review
- SARS-CoV-2 infection of human cortical cells is influenced by the interaction between aneuploidy and biological sex: insights from a Down syndrome in vitro model.Acta neuropathologica · 2025Article
- Copy number normalization distinguishes differential signals driven by copy number differences in ATAC-seq and ChIP-seq.BMC genomics · 2025Article
- The immunogenetic basis of severe herpes simplex infections in neonates and children: a review.Pediatric research · 2025Review
- Impaired airway epithelial miR-155/BACH1/NRF2 axis and hypoxia gene expression during RSV infection in children with down syndrome.Frontiers in pediatrics · 2025Article
- DYRK1A in blood and immune function: implications in leukemia, inflammatory disorders, infection and Down syndrome.Frontiers in cell and developmental biology · 2025Review
- A novel STING variant triggers endothelial toxicity and SAVI disease.The Journal of experimental medicine · 2024Article
- Dysregulation of the Immune System in a Natural History Study of 1299 Individuals with Down Syndrome.Journal of clinical immunology · 2024Article
- Article
- Integrated longitudinal multiomics study identifies immune programs associated with acute COVID-19 severity and mortality.The Journal of clinical investigation · 2024Observational
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Down syndrome (DS) is typically caused by triplication of chromosome 21. Phenotypically, DS presents with developmental, neurocognitive, and immune features. Epidemiologically, individuals with DS have less frequent viral infection, but when present, these infections lead to more severe disease. The potent antiviral cytokine type I Interferon (IFN-I) receptor subunits IFNAR1 and IFNAR2 are located on chromosome 21. While increased IFNAR1/2 expression initially caused hypersensitivity to IFN-I, it triggered excessive negative feedback. This led to a hypo-response to subsequent IFN-I stimuli and an ensuing viral susceptibility in DS compared to control cells. Upregulation of IFNAR2 expression phenocopied the DS IFN-I dynamics independent of trisomy 21. CD14
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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.