Evidence map›Paper›PMID 31366013›Full record

ReviewInternational journal of molecular sciences2019

DNAM-1 Activating Receptor and Its Ligands: How Do Viruses Affect the NK Cell-Mediated Immune Surveillance during the Various Phases of Infection?

Loredana Cifaldi, Margherita Doria, Nicola Cotugno, Sonia Zicari, Caterina Cancrini, Paolo Palma, Paolo Rossi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.8field-weighted citation impact, top 14% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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  5. HIV-1 manipulates CD96 on CD4Science advances · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Loredana CifaldiAcademic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy. loredana.cifaldi@opbg.net.
Margherita DoriaAcademic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.ORCID 0000-0001-5533-0304
Nicola CotugnoAcademic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.
Sonia ZicariAcademic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.
Caterina CancriniAcademic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.
Paolo PalmaAcademic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.ORCID 0000-0002-3066-4719
Paolo RossiAcademic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.
Bambino Gesù Children's Hospital · ITUniversity of Rome Tor Vergata · IT

Funding

Ricerca Corrente Ospedale Pediatrico Bambino Gesù noneRicerca Finalizzata from Italian Ministry of Health RF-2016-02363642
6 · The paper itself

Abstract

Natural Killer (NK) cells play a critical role in host defense against viral infections. The mechanisms of recognition and killing of virus-infected cells mediated by NK cells are still only partially defined. Several viruses induce, on the surface of target cells, the expression of molecules that are specifically recognized by NK cell-activating receptors. The main NK cell-activating receptors involved in the recognition and killing of virus-infected cells are NKG2D and DNAM-1. In particular, ligands for DNAM-1 are nectin/nectin-like molecules involved also in mechanisms allowing viral infection. Viruses adopt several immune evasion strategies, including those affecting NK cell-mediated immune surveillance, causing persistent viral infection and the development of virus-associated diseases. The virus's immune evasion efficacy depends on molecules differently expressed during the various phases of infection. In this review, we overview the molecular strategies adopted by viruses, specifically cytomegalovirus (CMV), human immunodeficiency virus (HIV-1), herpes virus (HSV), Epstein-Barr virus (EBV) and hepatitis C virus (HCV), aiming to evade NK cell-mediated surveillance, with a special focus on the modulation of DNAM-1 activating receptor and its ligands in various phases of the viral life cycle. The increasing understanding of mechanisms involved in the modulation of activating ligands, together with those mediating the viral immune evasion strategies, would provide critical tools leading to design novel NK cell-based immunotherapies aiming at viral infection control, thus improving cure strategies of virus-associated diseases.

Indexed as

Immunologic SurveillanceAnimalsAntigens, Differentiation, T-LymphocyteHumansKiller Cells, NaturalNectinsT Lineage-Specific Activation Antigen 1Virus DiseasesVirus ReplicationAntigens, Differentiation, T-LymphocyteNectinsT Lineage-Specific Activation Antigen 1activating ligandsDNAM-1immune surveillanceNectin-2NK cellsPVRviral life cycle phasesviruses

Identifiers

PMID31366013
PMCPMC6695959
OpenAlexW2966688037

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.