ArticleScience (New York, N.Y.)2013
Blockade of chronic type I interferon signaling to control persistent LCMV infection.
Article in Science (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 489 papers, 1 of them a synthesis that pooled 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.
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
489 citing papers in PubMed, 1 synthesis or guideline pooled it, 700 citations in OpenAlex.
- Transcriptional insights into the CD8Journal of translational medicine · 2020Pooled it
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- Integrative Bulk and Single-Cell Profiling of Premanufacture T-cell Populations Reveals Factors Mediating Long-Term Persistence of CAR T-cell Therapy.Cancer discovery · 2021Trial
- Immunomodulation Induced During Interferon-α Therapy Impairs the Anti-HBV Immune Response Through CD24Frontiers in immunology · 2020Trial
- The transcription factor IRF8 drives tumor-specific exhaustion in CD8+ T cells.The Journal of experimental medicine · 2026Article
- Adaptive resistance in cancer immunotherapy.Cellular & molecular immunology · 2026Review
- A novel FcγRIIa-TRIM54-STAT2 axis negatively regulates type I interferon signaling and promotes viral susceptibility in human monocytes.Journal of virology · 2026Article
- Cytolysis limits IFN-I and effector memory CD8 T cells after viral vector vaccination.Molecular therapy. Nucleic acids · 2026Article
- Jump-starting the T cell response in established tumors.bioRxiv : the preprint server for biology · 2026Article
- Beyond suppression: the paradox of JAK inhibitors as amplifiers of cancer immunotherapy.Nature reviews. Immunology · 2026Review
- Pan-cancer single-cell atlases of mouse and human tumor-associated dendritic cells.Nature communications · 2026Article
- Transcriptomic evidence of CD8⁺ T-cell exhaustion-like phenotype and mitochondrial impairment underlying immune dysregulation in feline chronic gingivostomatitis.Scientific reports · 2026Article
- Persistent IFN-I signaling inhibits mitochondrial oxidative metabolism in CD8Cellular & molecular immunology · 2026Article
- Selective depletion of virus-specific CD8 T cells from the liver after PD-1 therapy with Fc-intact antibody during chronic infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Chronic infection perturbs the affinity hierarchy of antiviral B cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Regulated necrosis at the crossroads of liver inflammation and cancer development.Nature reviews. Gastroenterology & hepatology · 2026Review
- Functional Type I and Type II interferon crosstalk restricts progenitor exhausted CD8 T cells through spatial exclusion and checkpoint enforcement.bioRxiv : the preprint server for biology · 2026Article
- Primed to overreact: virus-induced IFN contributes to antibody-mediated anaphylaxis.The Journal of clinical investigation · 2026Article
- Early sex-related transcriptional differences in CD8Frontiers in immunology · 2026Article
429 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Type I interferons (IFN-I) are critical for antiviral immunity; however, chronic IFN-I signaling is associated with hyperimmune activation and disease progression in persistent infections. We demonstrated in mice that blockade of IFN-I signaling diminished chronic immune activation and immune suppression, restored lymphoid tissue architecture, and increased immune parameters associated with control of virus replication, ultimately facilitating clearance of the persistent infection. The accelerated control of persistent infection induced by blocking IFN-I signaling required CD4 T cells and was associated with enhanced IFN-γ production. Thus, we demonstrated that interfering with chronic IFN-I signaling during persistent infection redirects the immune environment to enable control of infection.
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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.