ArticleThe Journal of experimental medicine2004
The cytomegalovirus m155 gene product subverts natural killer cell antiviral protection by disruption of H60-NKG2D interactions.
Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 143 citations in OpenAlex.
- Recognition of Self and Viral Ligands by NK Cell Receptors.Immunological reviews · 2025Review
- Review
- The m15 Locus of Murine Cytomegalovirus Modulates Natural Killer Cell Responses to Promote Dissemination to the Salivary Glands and Viral Shedding.Pathogens (Basel, Switzerland) · 2021Article
- Recent Approaches and Strategies in the Generation of Anti-human Cytomegalovirus Vaccines.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Review
- Modulation of innate and adaptive immunity by cytomegaloviruses.Nature reviews. Immunology · 2020Review
- Herpesvirus Evasion of Natural Killer Cells.Journal of virology · 2018Review
- Murine CMV Expressing the High Affinity NKG2D Ligand MULT-1: A Model for the Development of Cytomegalovirus-Based Vaccines.Frontiers in immunology · 2018Article
- Inhibition of Murine Cytomegalovirus Infection in Animals by RNase P-Associated External Guide Sequences.Molecular therapy. Nucleic acids · 2017Article
- Dysregulated cellular functions and cell stress pathways provide critical cues for activating and targeting natural killer cells to transformed and infected cells.Immunological reviews · 2017Review
- Parallel Evolution of Chemokine Binding by Structurally Related Herpesvirus Decoy Receptors.Structure (London, England : 1993) · 2016Article
- Increased Bacterial Load and Expression of Antimicrobial Peptides in Skin of Barrier-Deficient Mice with Reduced Cancer Susceptibility.The Journal of investigative dermatology · 2016Article
- NKG2D Receptor and Its Ligands in Host Defense.Cancer immunology research · 2015Review
- Modulation of Clr Ligand Expression and NKR-P1 Receptor Function during Murine Cytomegalovirus Infection.Journal of innate immunity · 2015Article
- MCMV avoidance of recognition and control by NK cells.Seminars in immunopathology · 2014Review
- Cytomegalovirus m154 hinders CD48 cell-surface expression and promotes viral escape from host natural killer cell control.PLoS pathogens · 2014Article
- Structural basis for recognition of cellular and viral ligands by NK cell receptors.Frontiers in immunology · 2014Review
- The p36 isoform of murine cytomegalovirus m152 protein suffices for mediating innate and adaptive immune evasion.Viruses · 2013Article
- Inflammatory cytokine-mediated evasion of virus-induced tumors from NK cell control.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Natural killer (NK) cells are an important early mediator of host immunity to murine cytomegalovirus (MCMV) infection. However, MCMV has evolved mechanisms to elude recognition and clearance by NK cells. We have identified an MCMV immune evasion protein that impairs NKG2D-mediated NK cell antiviral activity. Infection of BALB/c 3T3 cells with the Smith strain of MCMV resulted in strong down-regulation of H60, a high affinity ligand for NKG2D, from the surface of virus-infected cells. The MCMV m155 protein specifically down-regulated H60 without affecting expression of the other known NKG2D ligands, RAE-1 and MULT-1. Treatment with the proteasome inhibitors lactacystin or epoxomicin reversed m155 down-regulation of H60. An MCMV mutant virus lacking m155 was severely attenuated in BALB/c mice; however, treatment with neutralizing anti-NKG2D monoclonal antibody or with NK-depleting anti-asialo GM1 antisera restored virulence of the mutant virus. Thus, down-regulation of H60 by m155 is a powerful mechanism of inhibiting NKG2D-mediated antiviral function.
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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.