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Viruses
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Natural Killer Cell in Viral Infection
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Natural Killer Cell in Viral Infection

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 2326

Special Issue Editor

Prof. Dr. Min Fang

E-Mail Website
Guest Editor
School of Life Sciences, Henan University, Kaifeng 475004, China
Interests: the role and mechanism of NK cells in viral infection; mechanism of NK in controlling early virus replication and transmission; the mechanisms by which NK cells recognize virus infected cells; the role of different subgroups of NK cell during viral infection; the functional change of NK cells with aging; the impact and mechanism of NK cell response on subsequent T and B cell responses

Special Issue Information

Dear Colleagues,

NK cells are a critical cell population in innate immunity, playing roles in antiviral and anti-tumor immunity. Nevertheless, how NK cells function to address these challenges remains poorly understood. Meanwhile, NK cell function declines with aging, which has a critical impact on overall immunity in the elderly. Understanding the molecular and cellular mechanisms involved in NK cell activation, expansion, and memory will reveal possible pathways to enhance NK cell function and enhance immunity against viral infections. The goal of this Special Issue of Viruses is to explore interactions between NK cells and viruses.

Primary research and review articles pertaining to virus interactions with NK and NK-related immune populations are invited. Topics of interest include, but are not limited to, the following:

  1. Innate recognition of NK cells during viral infection;
  2. Generation and regulation of NK cell memory;
  3. Defects in NK cell function with aging and viral infection.

Prof. Dr. Min Fang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • NK cells
  • viral infection
  • innate immune responses
  • signaling pathway
  • virus replication and transmission
  • NK cell receptors

Published Papers (3 papers)

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Research

12 pages, 1079 KiB  
Communication
NTB-A and 2B4 Natural Killer Cell Receptors Modulate the Capacity of a Cocktail of Non-Neutralizing Antibodies and a Small CD4-Mimetic to Eliminate HIV-1-Infected Cells by Antibody-Dependent Cellular Cytotoxicity
by Lorie Marchitto, Alexandra Tauzin, Mehdi Benlarbi, Guillaume Beaudoin-Bussières, Katrina Dionne, Étienne Bélanger, Debashree Chatterjee, Catherine Bourassa, Halima Medjahed, Derek Yang, Ta-Jung Chiu, Hung-Ching Chen, Amos B. Smith III, Jonathan Richard and Andrés Finzi
Viruses 2024, 16(7), 1167; https://doi.org/10.3390/v16071167 (registering DOI) - 20 Jul 2024
Abstract
Natural Killer (NK) cells have the potential to eliminate HIV-1-infected cells by antibody-dependent cellular cytotoxicity (ADCC). NK cell activation is tightly regulated by the engagement of its inhibitory and activating receptors. The activating receptor CD16 drives ADCC upon binding to the Fc portion [...] Read more.
Natural Killer (NK) cells have the potential to eliminate HIV-1-infected cells by antibody-dependent cellular cytotoxicity (ADCC). NK cell activation is tightly regulated by the engagement of its inhibitory and activating receptors. The activating receptor CD16 drives ADCC upon binding to the Fc portion of antibodies; NK cell activation is further sustained by the co-engagement of activating receptors NTB-A and 2B4. During HIV-1 infection, Nef and Vpu accessory proteins contribute to ADCC escape by downregulating the ligands of NTB-A and 2B4. HIV-1 also evades ADCC by keeping its envelope glycoproteins (Env) in a “closed” conformation which effectively masks epitopes recognized by non-neutralizing antibodies (nnAbs) which are abundant in the plasma of people living with HIV. To achieve this, the virus uses its accessory proteins Nef and Vpu to downregulate the CD4 receptor, which otherwise interacts with Env and exposes the epitopes recognized by nnAbs. Small CD4-mimetic compounds (CD4mc) have the capacity to expose these epitopes, thus sensitizing infected cells to ADCC. Given the central role of NK cell co-activating receptors NTB-A and 2B4 in Fc-effector functions, we studied their contribution to CD4mc-mediated ADCC. Despite the fact that their ligands are partially downregulated by HIV-1, we found that both co-activating receptors significantly contribute to CD4mc sensitization of HIV-1-infected cells to ADCC. Full article
(This article belongs to the Special Issue Natural Killer Cell in Viral Infection)
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11 pages, 4842 KiB  
Article
Cytokine Response of Natural Killer Cells to Hepatitis B Virus Infection Depends on Monocyte Co-Stimulation
by Paul Kupke, Johanna Brucker, Jochen M. Wettengel, Ulrike Protzer, Jürgen J. Wenzel, Hans J. Schlitt, Edward K. Geissler and Jens M. Werner
Viruses 2024, 16(5), 741; https://doi.org/10.3390/v16050741 - 8 May 2024
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Abstract
Hepatitis B virus (HBV) is a major driver of chronic hepatic inflammation, which regularly leads to liver cirrhosis or hepatocellular carcinoma. Immediate innate immune cell response is crucial for the rapid clearance of the infection. Here, natural killer (NK) cells play a pivotal [...] Read more.
Hepatitis B virus (HBV) is a major driver of chronic hepatic inflammation, which regularly leads to liver cirrhosis or hepatocellular carcinoma. Immediate innate immune cell response is crucial for the rapid clearance of the infection. Here, natural killer (NK) cells play a pivotal role in direct cytotoxicity and the secretion of antiviral cytokines as well as regulatory function. The aim of this study was to further elucidate NK cell responses triggered by an HBV infection. Therefore, we optimized HBV in vitro models that reliably stimulate NK cells using hepatocyte-like HepG2 cells expressing the Na+-taurocholate co-transporting polypeptide (NTCP) and HepaRG cells. Immune cells were acquired from healthy platelet donors. Initially, HepG2-NTCP cells demonstrated higher viral replication compared to HepaRG cells. Co-cultures with immune cells revealed increased production of interferon-γ and tumor necrosis factor-α by NK cells, which was no longer evident in isolated NK cells. Likewise, the depletion of monocytes and spatial separation from target cells led to the absence of the antiviral cytokine production of NK cells. Eventually, the combined co-culture of isolated NK cells and monocytes led to a sufficient cytokine response of NK cells, which was also apparent when communication between the two immune cell subpopulations was restricted to soluble factors. In summary, our study demonstrates antiviral cytokine production by NK cells in response to HBV+ HepG2-NTCP cells, which is dependent on monocyte bystander activation. Full article
(This article belongs to the Special Issue Natural Killer Cell in Viral Infection)
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17 pages, 4760 KiB  
Article
Galectin-3-ITGB1 Signaling Mediates Interleukin 10 Production of Hepatic Conventional Natural Killer Cells in Hepatitis B Virus Transgenic Mice and Correlates with Hepatocellular Carcinoma Progression in Patients
by Yongyan Chen, Wendi Zhang, Min Cheng, Xiaolei Hao, Haiming Wei, Rui Sun and Zhigang Tian
Viruses 2024, 16(5), 737; https://doi.org/10.3390/v16050737 - 7 May 2024
Viewed by 890
Abstract
Background and Aims: The outcomes of HBV infections are related to complex immune imbalances; however, the precise mechanisms by which HBV induces immune dysfunction are not well understood. Methods: HBV transgenic (HBs-Tg) mice were used to investigate intrahepatic NK cells in two distinct [...] Read more.
Background and Aims: The outcomes of HBV infections are related to complex immune imbalances; however, the precise mechanisms by which HBV induces immune dysfunction are not well understood. Methods: HBV transgenic (HBs-Tg) mice were used to investigate intrahepatic NK cells in two distinct subsets: conventional NK (cNK) and liver-resident NK (LrNK) cells during a chronic HBV infection. Results: The cNK cells, but not the LrNK cells, were primarily responsible for the increase in the number of bulk NK cells in the livers of ageing HBs-Tg mice. The hepatic cNK cells showed a stronger ability to produce IL-10, coupled with a higher expression of CD69, TIGIT and PD-L1, and lower NKG2D expression in ageing HBs-Tg mice. A lower mitochondrial mass and membrane potential, and less polarized localization were observed in the hepatic cNK cells compared with the splenic cNK cells in the HBs-Tg mice. The enhanced galectin-3 (Gal-3) secreted from HBsAg+ hepatocytes accounted for the IL-10 production of hepatic cNK cells via ITGB1 signaling. For humans, LGALS3 and ITGB1 expression is positively correlated with IL-10 expression, and negatively correlated with the poor clinical progression of HCC. Conclusions: Gal-3-ITGB1 signaling shapes hepatic cNK cells but not LrNK cells during a chronic HBV infection, which may correlate with HCC progression. Full article
(This article belongs to the Special Issue Natural Killer Cell in Viral Infection)
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