ArticleJournal of virology2013
Lymphoid-tissue stromal cells coordinate innate defense to cytomegalovirus.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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
21 citing papers in PubMed, 28 citations in OpenAlex.
- Lymphotoxin-LIGHT pathway regulates the interferon signature in rheumatoid arthritis.PloS one · 2014Trial
- Dendritic Cells and Their Crucial Role in Modulating Innate Lymphoid Cells for Treating and Preventing Infectious Diseases.Pathogens (Basel, Switzerland) · 2025Review
- Type I interferon regulation of group I ILC subsets during both homeostasis and cytomegalovirus infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Tissue-specific features of innate lymphoid cells in antiviral defense.Cellular & molecular immunology · 2024Review
- Late-rising CD4 T cells resolve mouse cytomegalovirus persistent replication in the salivary gland.PLoS pathogens · 2024Article
- Vaccine Vectors Harnessing the Power of Cytomegaloviruses.Vaccines · 2019Review
- Life-long control of cytomegalovirus (CMV) by T resident memory cells in the adipose tissue results in inflammation and hyperglycemia.PLoS pathogens · 2019Article
- Chronic alcohol consumption exacerbates murine cytomegalovirus infection via impairing nonspecific and specific NK activation in mice.FASEB bioAdvances · 2019Article
- Chronic alcohol consumption exacerbates murine cytomegalovirus infection via impairing nonspecific and specific NK activation in mice.FASEB bioAdvances · 2019Article
- Control of primary mouse cytomegalovirus infection in lung nodular inflammatory foci by cooperation of interferon-gamma expressing CD4 and CD8 T cells.PLoS pathogens · 2018Article
- Cytomegalovirus: Shape-Shifting the Immune System.Journal of immunology (Baltimore, Md. : 1950) · 2018Review
- Navigating the Host Cell Response during Entry into Sites of Latent Cytomegalovirus Infection.Pathogens (Basel, Switzerland) · 2018Review
- Murine Cytomegalovirus Disrupts Splenic Dendritic Cell SubsetsFrontiers in immunology · 2017Article
- The Mouse Cytomegalovirus Gene m42 Targets Surface Expression of the Protein Tyrosine Phosphatase CD45 in Infected Macrophages.PLoS pathogens · 2016Article
- cGAS-STING Signaling Regulates Initial Innate Control of Cytomegalovirus Infection.Journal of virology · 2016Article
- Cytomegalovirus-Specific CD4 T Cells Are Cytolytic and Mediate Vaccine Protection.Journal of virology · 2016Article
- Cardif (MAVS) Regulates the Maturation of NK Cells.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Inhibition of the TRAIL death receptor by CMV reveals its importance in NK cell-mediated antiviral defense.PLoS pathogens · 2014Article
- Distinct requirements for activation of NKT and NK cells during viral infection.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Neutrophils recruited by IL-22 in peripheral tissues function as TRAIL-dependent antiviral effectors against MCMV.Cell host & microbe · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
During mouse cytomegalovirus (MCMV) infection, the first wave of type I interferon (IFN-I) production peaks at ≈ 8 h. This IFN-I emanates from splenic stromal cells located in the marginal zone (MZ) and requires B cells that express lymphotoxin. The amount of IFN-I produced at these initial times is at least equivalent in magnitude to that produced later by dendritic cells (≈ 36 to 48 h), but the relative roles of these two IFN-I sources in regulating MCMV defense remain unclear. Here we show that IFN-I produced by MZ stromal cells dramatically restricts the first measurable burst of viral production, which occurs at ≈ 32 h. This primary innate control by IFN-I is partially mediated through the activation of natural killer (NK) cells, which produce gamma interferon in an IFN-I-dependent fashion, and is independent of Ly49H. Strikingly, MCMV production in the spleens of immunocompetent mice never increases at times after 32 h. These results highlight the critical importance of lymphoid-tissue stromal cells in orchestrating the earliest phase of innate defense to MCMV infection, capping replication levels, and blocking spread until infection is ultimately controlled.
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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.