Expansion of 2B4+ natural killer (NK) cells and decrease in NKp46+ NK cells in response to influenza

Jost, Stéphanie; Reardon, Jeff; Peterson, Eric C.; Poole, Danielle; Bosch, Ronald J.; Alter, Galit; Altfeld, Marcus

doi:10.1111/j.1365-2567.2010.03394.x

Cited by 36 publications

(33 citation statements)

References 53 publications

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“…However, despite these observations, the mechanism underlying this downregulation has remained elusive. Reductions in NKp46 expression in HIV-unrelated in vitro experiments was demonstrated to occur upon activation and, in some cases, after direct ligation of the receptor (30,39). However, infection of CD4 + T lymphocytes with HIV does not induce the expression of NKp46 ligands (31).…”

Section: Discussionmentioning

confidence: 99%

“…The level of NKp46 expressed on the NK cell surface is associated with the magnitude of the response elicited upon ligation (15). Chronic HIV infection that induces ongoing activation of NK cells due to ADCC would be expected to elicit in vivo phenotypic and functional changes in NK cells similar to those observed after in vitro activation (i.e., reduced CD16 expression, hyporesponsiveness, and reduced NKp46 expression) (26)(27)(28)(29)39). Indeed, HIV infection results in a set of dysfunctional NK cell changes similar to that observed after CD16-mediated activation in vitro (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22).…”

Section: Discussionmentioning

confidence: 99%

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Anti-HIV Antibody–Dependent Activation of NK Cells Impairs NKp46 Expression

Parsons

Tang

Jegaskanda

et al. 2014

The Journal of Immunology

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There is much interest in the potential of Ab-dependent cellular cytotoxicity (ADCC) to slow disease progression following HIV infection. Despite several studies demonstrating a positive association between ADCC and slower disease progression, it is possible that continued stimulation of NK cells by ADCC during chronic HIV infection could render these cells dysfunctional. Indeed, activation of NK cells by ADCC results in matrix metalloproteinase–induced reductions in CD16 expression and activation refractory periods. In addition, ex vivo analyses of NK cells from HIV-infected individuals revealed other alterations in phenotype, such as decreased expression of the activating NKp46 receptor that is essential for NK-mediated antitumor responses and immunity from infection. Because NKp46 shares a signaling pathway with CD16, we hypothesized that activation-induced downregulation of both receptors could be controlled by a common mechanism. We found that activation of NK cells by anti-HIV or anti-CD16 Abs resulted in NKp46 downregulation. The addition of a matrix metalloproteinase inhibitor attenuated NKp46 downregulation following NK cell activation by anti-HIV Abs. Consequently, these results suggest that continued stimulation through CD16 has the potential to impair natural cytotoxicity via attenuation of NKp46-dependent signals.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Anti-HIV Antibody–Dependent Activation of NK Cells Impairs NKp46 Expression

Parsons

Tang

Jegaskanda

et al. 2014

The Journal of Immunology

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“…With regard to NCRs, Notch was proposed as a key positive regulator for mucosal ILC3 in mice (21), whereas TGF-b can modulate human NKp30 expression in vitro (29). NKp46 expression is reduced in cancer patients (30) and during influenza and HIV infection (30)(31)(32) + GFP + cells cultured on OP9 cells, whereas GFP expression remained constant on OP9-DL1 cells (Fig. 4D).…”

Section: Signals That Modulate Nkp46 Expression On Intestinal Ilc3mentioning

confidence: 99%

Phenotypic and Functional Plasticity of Murine Intestinal NKp46+ Group 3 Innate Lymphoid Cells

Verrier

Satoh-Takayama

Serafini

et al. 2016

The Journal of Immunology

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Group 3 innate lymphoid cells (ILC3) actively participate in mucosal defense and homeostasis through prompt secretion of IL-17A, IL-22, and IFN-γ. Reports identify two ILC3 lineages: a CCR6+T-bet− subset that appears early in embryonic development and promotes lymphoid organogenesis and a CCR6−T-bet+ subset that emerges after microbial colonization and harbors NKp46+ ILC3. We demonstrate that NKp46 expression in the ILC3 subset is highly unstable. Cell fate mapping using Ncr1CreGFP × Rosa26RFP mice revealed the existence of an intestinal RFP+ ILC3 subset (Ncr1FM) lacking NKp46 expression at the transcript and protein levels. Ncr1FM ILC3 produced more IL-22 and were distinguishable from NKp46+ ILC3 by differential CD117, CD49a, DNAX accessory molecule-1, and, surprisingly, CCR6 expression. Ncr1FM ILC3 emerged after birth and persisted in adult mice following broad-spectrum antibiotic treatment. These results identify an unexpected phenotypic instability within NKp46+ ILC3 that suggests a major role for environmental signals in tuning ILC3 functional plasticity.

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“…Over the past decade, several studies have addressed the role of NK cells and their receptors involved in the induction of cell killing in influenza virus infections (8,9,10,12,15,19,22,23). Because NK lymphocytes do not require prior sensitization to exert their lytic effects on infected cells, they may have a key protective role against emergent pathogens or new variants or strains of different viruses.…”

Section: Discussionmentioning

confidence: 99%

Influenza Virus Infection but Not H1N1 Influenza Virus Immunization Is Associated with Changes in Peripheral Blood NK Cell Subset Levels

Juárez-Reyes

Noyola

Monsiváis‐Urenda

et al. 2013

Clin Vaccine Immunol

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The innate immune system constitutes the first line of defense against viral agents, and NK cells seem to have an important protective role during the early phases of influenza virus infections. We decided to assess the levels of NK and NKT lymphocytes and the expression levels of different membrane receptors (NKp44, NKp46, NKG2A, killer cell immune-like receptor [KIR] 3DL1/ DS1, KIR2DL1/DS1, and CD161) in peripheral blood samples of patients with influenza (n ‫؍‬ 17) and healthy individuals immunized against this virus (seasonal and [H1N1]pdm2009 influenza vaccines; n ‫؍‬ 15 and 12, respectively). Blood samples were obtained from all individuals, and NK and NKT cell subsets were analyzed by multiparametric flow cytometry. We found that the patients with severe influenza (n ‫؍‬ 9) showed significant increases in the percentages of NKp46 ؉ NKp44 ؉ NK cells and the proportions of NK and NKT lymphocytes expressing KIR2DL1 and KIR3DL1 and reductions in the percentages of NKp46 ؉ NKp44؊ NK cells compared to those in the healthy controls (n ‫؍‬ 27). In contrast, influenza immunization, against either the seasonal or the pandemic H1N1 virus, was not associated with important changes in the levels of NK and NKT lymphocytes or the expression levels of the different receptors by these cells. Our data suggest that severe influenza is associated with important and complex alterations on NK cells, which might contribute to the pathogenesis of this condition.

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Expansion of 2B4+ natural killer (NK) cells and decrease in NKp46+ NK cells in response to influenza

Cited by 36 publications

References 53 publications

Anti-HIV Antibody–Dependent Activation of NK Cells Impairs NKp46 Expression

Anti-HIV Antibody–Dependent Activation of NK Cells Impairs NKp46 Expression

Phenotypic and Functional Plasticity of Murine Intestinal NKp46+ Group 3 Innate Lymphoid Cells

Influenza Virus Infection but Not H1N1 Influenza Virus Immunization Is Associated with Changes in Peripheral Blood NK Cell Subset Levels

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