NK Cells and their Receptors during Viral Infections

Marcenaro, Emanuela; Carlomagno, Simona; Pesce, Silvia; Chiesa, Mariella Della; Parolini, Silvia; Moretta, Alessandro; Sivori, Simona

doi:10.2217/imt.11.99

Cited by 25 publications

(22 citation statements)

References 119 publications

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“…Although, at first glance, incomplete downregulation may seem to be disadvantageous for the virus in its attempt to escape from CTLs, it will prevent the action of natural killer (NK) cells. Cell surface expression of MHC-I molecules provides inhibitory signals to NK cells, and modulation of MHC-I presentation could sensitize infected cells for NK-mediated cytotoxicity (25). Avoiding NK cell responses by selectively downregulating MHC-I alleles, which do not provide inhibitory signals, or by expressing nonfunctional MHC-I decoys is known for beta-and gammaherpesviruses (14), and similar functions may be at play during alphaherpesvirus infections as well.…”

Section: Discussionmentioning

confidence: 99%

Identification and Characterization of Equine Herpesvirus Type 1 pUL56 and Its Role in Virus-Induced Downregulation of Major Histocompatibility Complex Class I

Feineis

Osterrieder

et al. 2012

J Virol

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bMajor histocompatibility complex class I (MHC-I) molecules play an important role in host immunity to infection by presenting antigenic peptides to cytotoxic T lymphocytes (CTLs), which recognize and destroy virus-infected cells. Members of the Herpesviridae have developed multiple mechanisms to avoid CTL recognition by virtue of downregulation of MHC-I on the cell surface. We report here on an immunomodulatory protein involved in this process, pUL56, which is encoded by ORF1 of equine herpesvirus type 1 (EHV-1), an alphaherpesvirus. We show that EHV-1 pUL56 is a phosphorylated early protein which is expressed as different forms and predominantly localizes to Golgi membranes. In addition, the transmembrane (TM) domain of the type II membrane protein was shown to be indispensable for correct subcellular localization and a proper function. pUL56 by itself is not functional with respect to interference with MHC-I and likely needs another unidentified viral protein(s) to perform this action. Surprisingly, pUL49.5, an inhibitor of the transporter associated with antigen processing (TAP) and encoded by EHV-1 and related viruses, appeared not to be required for pUL56-induced early MHC-I downmodulation in infected cells. In conclusion, our data identify a new immunomodulatory protein, pUL56, involved in MHC-I downregulation which is unable to perform its function outside the context of viral infection.

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Section: Discussionmentioning

confidence: 99%

Identification and Characterization of Equine Herpesvirus Type 1 pUL56 and Its Role in Virus-Induced Downregulation of Major Histocompatibility Complex Class I

Feineis

Osterrieder

et al. 2012

J Virol

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“…[11][12][13] NK lymphocytes constitute an important cell subset in the immune response against intracellular pathogens and virally infected cells. 14 Functioning of NK cells is controlled by an array of different activating and inhibitory receptors 15 that, on engagement by specific cell ligands, can either induce or suppress the process of killing. During early viral infection, STAT1 expression is dramatically induced and NK cell activity can be influenced by STAT1 phosphorylation.…”

Section: Lymphoid Tissuementioning

confidence: 99%

Impaired natural killer cell functions in patients with signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations

Tabellini

Vairo

Scomodon

et al. 2017

Journal of Allergy and Clinical Immunology

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“…The “on signal” exerted by aNKRs to trigger NK cell killing depends on the induced expression of putative ligands for activating receptors on virally infected target cells. The recognition of these specific ligands is required for the engagement of aNKR-mediated downstream pathways associated with the NK cell release of lytic granules (4–13). …”

Section: Introductionmentioning

confidence: 99%

NK Cell Subset Redistribution during the Course of Viral Infections

2014

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Natural killer (NK) cells are important effectors of innate immunity that play a critical role in the control of human viral infections. Indeed, given their capability to directly recognize virally infected cells without the need of specific antigen presentation, NK cells are on the first line of defense against these invading pathogens. By establishing cellular networks with a variety of cell types such as dendritic cells, NK cells can also amplify anti-viral adaptive immune responses. In turn, viruses evolved and developed several mechanisms to evade NK cell-mediated immune activity. It has been reported that certain viral diseases, including human immunodeficiency virus-1 as well as human cytomegalovirus infections, are associated with a pathologic redistribution of NK cell subsets in the peripheral blood. In particular, it has been observed the expansion of unconventional CD56neg NK cells, whose effector functions are significantly impaired as compared to that of conventional CD56pos NK cells. In this review, we address the impact of these two chronic viral infections on the functional and phenotypic perturbations of human NK cell compartment.

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NK Cells and their Receptors during Viral Infections

Cited by 25 publications

References 119 publications

Identification and Characterization of Equine Herpesvirus Type 1 pUL56 and Its Role in Virus-Induced Downregulation of Major Histocompatibility Complex Class I

Identification and Characterization of Equine Herpesvirus Type 1 pUL56 and Its Role in Virus-Induced Downregulation of Major Histocompatibility Complex Class I

Impaired natural killer cell functions in patients with signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations

NK Cell Subset Redistribution during the Course of Viral Infections

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