ArticleThe Journal of clinical investigation2017
HIV-antibody complexes enhance production of type I interferon by plasmacytoid dendritic cells.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 18 citations in OpenAlex.
- The emerging role of TLR7-mediated signaling in respiratory viral infections and autoimmune diseases.Cellular and molecular life sciences : CMLS · 2026Review
- ANKRD22 promotes resolution of psoriasiform skin inflammation by antagonizing NIK-mediated IL-23 production.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- The crucial regulatory role of type I interferon in inflammatory diseases.Cell & bioscience · 2023Review
- Research Progress of Dendritic Cell Surface Receptors and Targeting.Biomedicines · 2023Review
- Article
- Article
- People with HIV-1 demonstrate type 1 interferon refractoriness associated with upregulated USP18.Journal of virology · 2021Article
- The cGAS/STING Pathway: A Novel Target for Cancer Therapy.Frontiers in immunology · 2021Review
- Review
- HIV and the liver.Topics in antiviral medicine · 2019Article
- HIV-1 Infection and Type 1 Interferon: Navigating Through Uncertain Waters.AIDS research and human retroviruses · 2019Review
- Manipulation of Type I Interferon Signaling by HIV and AIDS-Associated Viruses.Journal of immunology research · 2019Review
- SLAMF7 Is a Critical Negative Regulator of IFN-α-Mediated CXCL10 Production in Chronic HIV Infection.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Identification of key genes and pathways in regulating immune‑induced diseases of dendritic cells by bioinformatic analysis.Molecular medicine reports · 2018Article
- Sustained IFN-I Expression during Established Persistent Viral Infection: A "Bad Seed" for Protective Immunity.Viruses · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Type I IFN production is essential for innate control of acute viral infection; however, prolonged high-level IFN production is associated with chronic immune activation in HIV-infected individuals. Although plasmacytoid DCs (pDCs) are a primary source of IFN, the mechanisms that regulate IFN levels following the acute phase are unknown. We hypothesized that HIV-specific Ab responses regulate late IFN production. We evaluated the mechanism through which HIV-activated pDCs produce IFN as well as how both monoclonal HIV-specific Abs and Abs produced in natural HIV infection modulated normal pDC sensing of HIV. We found that HIV-induced IFN production required TLR7 signaling, receptor-mediated entry, fusion, and viral uncoating, but not endocytosis or HIV life cycle stages after uncoating. Abs directed against the HIV envelope that do not interfere with CD4 binding markedly enhanced the IFN response, irrespective of their ability to neutralize CD4+ T cell infection. Ab-mediated enhancement of IFN production required Fc γ receptor engagement, bypassed fusion, and initiated signaling through both TLR7 and TLR9, which was not utilized in the absence of Ab. Polyclonal Abs isolated from HIV-infected subjects also enhanced pDC production of IFN in response to HIV. Our data provide an explanation for high levels of IFN production and immune activation in chronic HIV infection.
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.