Human herpesvirus-6 enhances natural killer cell cytotoxicity via IL-15.

Flamand, Louis; Stefănescu, I; Menezes, José

doi:10.1172/jci118557

Cited by 133 publications

(99 citation statements)

References 26 publications

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“…In the present report, we describe augmentation of NK (4,7,8,24,55) and antitumor (20,67) host defenses. Target cell death mediated by NK cells is mediated by two predominant mechanisms: the Ca2 ϩ -dependent release of perforin and granzymes (77) and production of members of the TNF family of death-inducing ligands, such as FasL (42,57), TNF alpha (77), and TRAIL.…”

Section: Discussionmentioning

confidence: 53%

Differential Effects of Interleukin-7 and Interleukin-15 on NK Cell Anti-Human Immunodeficiency Virus Activity

Lum

Schnepple

Nie

et al. 2004

J Virol

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Section: Discussionmentioning

confidence: 53%

Differential Effects of Interleukin-7 and Interleukin-15 on NK Cell Anti-Human Immunodeficiency Virus Activity

Lum

Schnepple

Nie

et al. 2004

J Virol

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“…It thus appears that IL-15 has potential roles in the development and maintenance of significant fractions of lymphocytes, including NK, NKT, TCR␥␦ i-IEL, and memory phenotype CD8 ϩ T cells. There have been several lines of evidence for IL-15 production in infection with various microbes, including M. tuberculosis (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35). We have demonstrated that IL-15 is involved in protection against infections with Escherichia coli (35) …”

Section: P Rotection Against Infection With Mycobacterium Tuberculosimentioning

confidence: 99%

Overexpression of IL-15 In Vivo Enhances Protection AgainstMycobacterium bovisBacillus Calmette-Guérin Infection Via Augmentation of NK and T Cytotoxic 1 Responses

Umemura

Nishimura

Hirose

et al. 2001

The Journal of Immunology

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To investigate the immunomodulating effects of IL-15 in vivo on mycobacterial infection, we used IL-15-transgenic (Tg) mice, which were recently constructed with cDNA-encoding secretable isoform of IL-15 precursor protein under the control of a MHC class I promoter. The IL-15-Tg mice exhibited resistance against infection with Mycobacterium bovis bacillus Calmette-Guérin (BCG), as assessed by bacteria growth. IFN-γ level in serum was significantly higher in IL-15-Tg mice than in non-Tg mice after BCG infection. NK cells were remarkably increased, and Ag-specific T cytotoxic 1 response mediated by CD8+ T cells producing IFN-γ was significantly augmented in the IL-15-Tg mice following BCG infection. Neutralization of endogenous IFN-γ by in vivo administration of anti-IFN-γ mAb deteriorated the clearance of the bacteria. Depletion of of NK cells or CD8+ T cells by invivo administration of anti-asialo-GM1 Ab or anti-CD8 mAb hampered the exclusion of bacteria. Thus, overexpression of IL-15 in vivo enhanced protection against BCG infection via augmentation of NK and T cytotoxic 1 responses.

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“…Given the ability of HHV-6 to modulate immune functions (33)(34)(35)(36)(37), eicosanoid synthesis modulation could play an important role in the pathogenesis of this virus, especially during the early steps of an infection. In the present work, we dissected the mechanisms by which HHV-6 up-regulates PGE 2 in monocytes/macrophages, and we identified the contribution of the different promoter elements in mediating COX-2 transcription.…”

mentioning

confidence: 99%

Activation of Monocyte Cyclooxygenase-2 Gene Expression by Human Herpesvirus 6

Janelle¹,

Gravel²,

Gosselin³

et al. 2002

Journal of Biological Chemistry

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Prostaglandin E 2 (PGE 2 ) is an arachidonic acid metabolite mainly produced by activated monocytes/macrophages (Mo/M) that display broad immunomodulatory activities. Several viruses capable of infecting Mo/M modulate PGE 2 synthesis in a way that favors the infection processes and the spread of virions. In the present work, we studied the effect of human herpesvirus 6 (HHV-6) infection of Mo/M on PGE 2 synthesis. Our results indicate that HHV-6 induces COX-2 gene expression and PGE 2 synthesis within a few hours of infection. We mapped the different promoter elements associated with COX-2 gene activation by HHV-6 to two cis-acting elements: a cyclic AMP-responsive element and an activator protein-1 element. HHV-6 immediate-early protein 2 was identified as a modulator of COX-2 gene expression in Mo/M. Finally, addition of PGE 2 to HHV-6-infected peripheral blood mononuclear cells cultures was found to increase significantly viral replication. Overall, these results further contribute to the immunomodulatory properties of HHV-6 and highlight a potential role for eicosanoids in the replication process of this virus.

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Human herpesvirus-6 enhances natural killer cell cytotoxicity via IL-15.

Abstract: The marked tropism of human herpesvirus-6 (HHV-6) for natural killer (NK) cells and T lymphocytes has led us to investigate the effect of HHV-6 on cellular cytotoxicity. We describe here how HHV-6 infection of peripheral blood mononuclear cells (

Cited by 133 publications

References 26 publications

Differential Effects of Interleukin-7 and Interleukin-15 on NK Cell Anti-Human Immunodeficiency Virus Activity

Differential Effects of Interleukin-7 and Interleukin-15 on NK Cell Anti-Human Immunodeficiency Virus Activity

Overexpression of IL-15 In Vivo Enhances Protection AgainstMycobacterium bovisBacillus Calmette-Guérin Infection Via Augmentation of NK and T Cytotoxic 1 Responses

Activation of Monocyte Cyclooxygenase-2 Gene Expression by Human Herpesvirus 6

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