ArticlePLoS pathogens2012
Interferon-alpha subtype 11 activates NK cells and enables control of retroviral infection.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 52 citations in OpenAlex.
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- Dietary lipid overload creates a suppressive environment that impedes the antiviral functions of NK cells.iScience · 2025Article
- IFNα Subtypes in HIV Infection and Immunity.Viruses · 2024Review
- Iron improves the antiviral activity of NK cells.Frontiers in immunology · 2024Article
- Differences in neuroinvasion and protective innate immune pathways between encephalitic California Serogroup orthobunyaviruses.PLoS pathogens · 2022Article
- Differential interferon-α subtype induced immune signatures are associated with suppression of SARS-CoV-2 infection.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Superior antiviral activity of IFNβ in genital HSV-1 infection.Frontiers in cellular and infection microbiology · 2022Article
- IFNα subtype-specific susceptibility of HBV in the course of chronic infection.Frontiers in immunology · 2022Article
- Potential role of IFN-α in COVID-19 patients and its underlying treatment options.Applied microbiology and biotechnology · 2021Review
- Induction of T Cell Senescence by Cytokine Induced Bystander Activation.Frontiers in aging · 2021Review
- Immunotherapy With Interferon α11, But Not Interferon Beta, Controls Persistent Retroviral Infection.Frontiers in immunology · 2021Article
- Qualitative Differences Between the IFNα subtypes and IFNβ Influence Chronic Mucosal HIV-1 Pathogenesis.PLoS pathogens · 2020Article
- Context Is Key: Delineating the Unique Functions of IFNα and IFNβ in Disease.Frontiers in immunology · 2020Review
- Friend retrovirus studies reveal complex interactions between intrinsic, innate and adaptive immunity.FEMS microbiology reviews · 2019Review
- Article
- Plasmacytoid dendritic cells respond to Epstein-Barr virus infection with a distinct type I interferon subtype profile.Blood advances · 2019Article
- Diverse Immunomodulatory Effects of Individual IFNα Subtypes on Virus-Specific CD8Frontiers in immunology · 2019Article
- ER intrabody-mediated inhibition of interferon α secretion by mouse macrophages and dendritic cells.PloS one · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The innate immune response mediated by cells such as natural killer (NK) cells is critical for the rapid containment of virus replication and spread during acute infection. Here, we show that subtype 11 of the type I interferon (IFN) family greatly potentiates the antiviral activity of NK cells during retroviral infection. Treatment of mice with IFN-α11 during Friend retrovirus infection (FV) significantly reduced viral loads and resulted in long-term protection from virus-induced leukemia. The effect of IFN-α11 on NK cells was direct and signaled through the type I IFN receptor. Furthermore, IFN-α11-mediated activation of NK cells enabled cytolytic killing of FV-infected target cells via the exocytosis pathway. Depletion and adoptive transfer experiments illustrated that NK cells played a major role in successful IFN-α11 therapy. Additional experiments with Mouse Cytomegalovirus infections demonstrated that the therapeutic effect of IFN-α11 is not restricted to retroviruses. The type I IFN subtypes 2 and 5, which bind the same receptor as IFN-α11, did not elicit similar antiviral effects. These results demonstrate a unique and subtype-specific activation of NK cells by IFN-α11.
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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.