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


Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
30 Jul 2019
Historique:
received: 04 07 2019
revised: 24 07 2019
accepted: 27 07 2019
entrez: 2 8 2019
pubmed: 2 8 2019
medline: 24 12 2019
Statut: epublish

Résumé

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.

Identifiants

pubmed: 31366013
pii: ijms20153715
doi: 10.3390/ijms20153715
pmc: PMC6695959
pii:
doi:

Substances chimiques

Antigens, Differentiation, T-Lymphocyte 0
CD226 antigen 0
Nectins 0

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Ricerca Corrente Ospedale Pediatrico Bambino Gesù
ID : none
Organisme : Ricerca Finalizzata from Italian Ministry of Health
ID : RF-2016-02363642

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Auteurs

Loredana Cifaldi (L)

Academic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy. loredana.cifaldi@opbg.net.

Margherita Doria (M)

Academic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.

Nicola Cotugno (N)

Academic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.

Sonia Zicari (S)

Academic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.

Caterina Cancrini (C)

Academic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.
Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.

Paolo Palma (P)

Academic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.

Paolo Rossi (P)

Academic Department of Pediatrics, Research Unit of Congenital and Perinatal Infection, Bambino Gesù Children's Hospital, 00165 Rome, Italy.
Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.

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