ArticleThe Journal of experimental medicine2016
Inflammatory monocytes and NK cells play a crucial role in DNAM-1-dependent control of cytomegalovirus infection.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- Natural killer cells against viral infection: from basic biology to immunotherapy.Precision clinical medicine · 2026Review
- Type I interferon regulation of group I ILC subsets during both homeostasis and cytomegalovirus infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- HCMV Variants Expressing ULBP2 Enhance the Function of Human NK Cells via its Receptor NKG2D.European journal of immunology · 2025Article
- Article
- M-CSF directs myeloid and NK cell differentiation to protect from CMV after hematopoietic cell transplantation.EMBO molecular medicine · 2023Article
- Membraneless Compartmentalization of Nuclear Assembly Sites during Murine Cytomegalovirus Infection.Viruses · 2023Article
- Immunosuppressive M2 TAMs represent a promising target population to enhance phagocytosis of ovarian cancer cellsFrontiers in immunology · 2023Article
- Increased blood CD226Annals of medicine · 2023Article
- TIGIT blockade repolarizes AML-associated TIGITJournal for immunotherapy of cancer · 2022Article
- Dynamic of Circulating DNAM-1+ Monocytes and NK Cells in Patients with STEMI Following Primary Percutaneous Coronary Intervention.Journal of cardiovascular development and disease · 2022Article
- CD226 knockout alleviates high-fat diet induced obesity by suppressing proinflammatory macrophage phenotype.Journal of translational medicine · 2021Article
- Poliovirus receptor (PVR)-like protein cosignaling network: new opportunities for cancer immunotherapy.Journal of experimental & clinical cancer research : CR · 2021Review
- Endosomal Phosphatidylinositol-3-Phosphate-Associated Functions Are Dispensable for Establishment of the Cytomegalovirus Pre-Assembly Compartment but Essential for the Virus Growth.Life (Basel, Switzerland) · 2021Article
- Vertically transferred maternal immune cells promote neonatal immunity against early life infections.Nature communications · 2021Article
- Transcriptome sequencing and multi-plex imaging of prostate cancer microenvironment reveals a dominant role for monocytic cells in progression.BMC cancer · 2021Article
- 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
- Viral Interactions with Adaptor-Protein Complexes: A Ubiquitous Trait among Viral Species.International journal of molecular sciences · 2021Review
- Novel immune-related genes in the tumor microenvironment with prognostic value in breast cancer.BMC cancer · 2021Article
- Quantitative Proteomics Analysis of Lytic KSHV Infection in Human Endothelial Cells Reveals Targets of Viral Immune Modulation.Cell reports · 2020Article
- NK Cells Augment Oncolytic Adenovirus Cytotoxicity in Ovarian Cancer.Molecular therapy oncolytics · 2020Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 4 countries.
Funding
Abstract
The poliovirus receptor (PVR) is a ubiquitously expressed glycoprotein involved in cellular adhesion and immune response. It engages the activating receptor DNAX accessory molecule (DNAM)-1, the inhibitory receptor TIGIT, and the CD96 receptor with both activating and inhibitory functions. Human cytomegalovirus (HCMV) down-regulates PVR expression, but the significance of this viral function in vivo remains unknown. Here, we demonstrate that mouse CMV (MCMV) also down-regulates the surface PVR. The m20.1 protein of MCMV retains PVR in the endoplasmic reticulum and promotes its degradation. A MCMV mutant lacking the PVR inhibitor was attenuated in normal mice but not in mice lacking DNAM-1. This attenuation was partially reversed by NK cell depletion, whereas the simultaneous depletion of mononuclear phagocytes abolished the virus control. This effect was associated with the increased expression of DNAM-1, whereas TIGIT and CD96 were absent on these cells. An increased level of proinflammatory cytokines in sera of mice infected with the virus lacking the m20.1 and an increased production of iNOS by inflammatory monocytes was observed. Blocking of CCL2 or the inhibition of iNOS significantly increased titer of the virus lacking m20.1. In this study, we have demonstrated that inflammatory monocytes, together with NK cells, are essential in the early control of CMV through the DNAM-1-PVR pathway.
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