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Cells
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Untangling the Cross-Talk between Immune Responses and Infection
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Untangling the Cross-Talk between Immune Responses and Infection

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 4618

Special Issue Editors

Dr. Eric Martinez

E-Mail Website
Guest Editor
Institut de Recherche en Infectiologie de Montpellier (IRIM), Université de Montpellier, CNRS, CEDEX 5, 34293 Montpellier, France
Interests: bacterial pathogens, host-pathogen interactions, innate immunity, autophagy
Special Issues, Collections and Topics in MDPI journals
Dr. Fabien Blanchet

E-Mail Website
Guest Editor
Institut de Recherche en Infectiologie de Montpellier (IRIM), Université de Montpellier, CNRS, 34090 Montpellier, France
Interests: dendritic cells; human immunodeficiency virus-1; innate immunity ; autophagy ;alarmins
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The recent COVID-19 outbreak, although surprising in its magnitude, was ultimately quite predictable and planned. This global health crisis revealed how fragile our hyperconnected world can suddenly be in the face of a pathogen that has no real borders. Even if amazing and unprecedented successes have been accomplished, thanks to the selflessness and resilience of caregivers and scientists, SARS-CoV2 nevertheless represents only one pathogen among thousands of other potentially existing ones, whether bacterial, viral, parasitic, or other. It is therefore becoming ever more critical to better understand the possible causes of the (re-)emergence of certain pathogens, in particular by untangling in more detail the mechanisms governing the host's immune response to these pathogens. Studies of each key step in the interaction of a pathogen with its host are therefore critically needed, ranging from endocytosis to intracellular trafficking, from the manipulation of signaling pathways to the modulation of the expression of specific host genes, from the control of cellular metabolic pathways to the regulation of specific enzymes important for the replication of the pathogen, or even from the localization of pathogen-derived proteins and genetic material until complete replication and further transmission towards other target cells. Those aspects of investigation are of major importance for pinpointing and characterizing the cellular mechanisms implicated and improving potential therapeutic approaches.

This volume of Cells invites scientists who are experts in this field to contribute original articles or reviews to increase our knowledge on host–pathogen interactions, which will allow readers to have an overview of the cellular mechanisms at play during the crosstalk between certain pathogens and host immune cells and also to appreciate the perspectives of therapeutic strategies aimed at preventing pathophysiological consequences.

Dr. Eric Martinez
Dr. Fabien Blanchet
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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.

Published Papers (4 papers)

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Research

13 pages, 2656 KiB  
Article
Further Characterization of the Antiviral Transmembrane Protein MARCH8
by Takuya Tada, Yanzhao Zhang, Dechuan Kong, Michiko Tanaka, Weitong Yao, Masanori Kameoka, Takamasa Ueno, Hideaki Fujita and Kenzo Tokunaga
Cells 2024, 13(8), 698; https://doi.org/10.3390/cells13080698 - 17 Apr 2024
Viewed by 821
Abstract
The cellular transmembrane protein MARCH8 impedes the incorporation of various viral envelope glycoproteins, such as the HIV-1 envelope glycoprotein (Env) and vesicular stomatitis virus G-glycoprotein (VSV-G), into virions by downregulating them from the surface of virus-producing cells. This downregulation significantly reduces the efficiency [...] Read more.
The cellular transmembrane protein MARCH8 impedes the incorporation of various viral envelope glycoproteins, such as the HIV-1 envelope glycoprotein (Env) and vesicular stomatitis virus G-glycoprotein (VSV-G), into virions by downregulating them from the surface of virus-producing cells. This downregulation significantly reduces the efficiency of virus infection. In this study, we aimed to further characterize this host protein by investigating its species specificity and the domains responsible for its antiviral activity, as well as its ability to inhibit cell-to-cell HIV-1 infection. We found that the antiviral function of MARCH8 is well conserved in the rhesus macaque, mouse, and bovine versions. The RING-CH domains of these versions are functionally important for inhibiting HIV-1 Env and VSV-G-pseudovirus infection, whereas tyrosine motifs are crucial for the former only, consistent with findings in human MARCH8. Through analysis of chimeric proteins between MARCH8 and non-antiviral MARCH3, we determined that both the N-terminal and C-terminal cytoplasmic tails, as well as presumably the N-terminal transmembrane domain, of MARCH8 are critical for its antiviral activity. Notably, we found that MARCH8 is unable to block cell-to-cell HIV-1 infection, likely due to its insufficient downregulation of Env. These findings offer further insights into understanding the biology of this antiviral transmembrane protein. Full article
(This article belongs to the Special Issue Untangling the Cross-Talk between Immune Responses and Infection)
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27 pages, 2573 KiB  
Article
The ZIKV NS5 Protein Aberrantly Alters the Tubulin Cytoskeleton, Induces the Accumulation of Autophagic p62 and Affects IFN Production: HDAC6 Has Emerged as an Anti-NS5/ZIKV Factor
by Silvia Pérez-Yanes, Iria Lorenzo-Sánchez, Romina Cabrera-Rodríguez, Jonay García-Luis, Rodrigo Trujillo-González, Judith Estévez-Herrera and Agustín Valenzuela-Fernández
Cells 2024, 13(7), 598; https://doi.org/10.3390/cells13070598 - 29 Mar 2024
Viewed by 995
Abstract
Zika virus (ZIKV) infection and pathogenesis are linked to the disruption of neurogenesis, congenital Zika syndrome and microcephaly by affecting neural progenitor cells. Nonstructural protein 5 (NS5) is the largest product encoded by ZIKV-RNA and is important for replication and immune evasion. Here, [...] Read more.
Zika virus (ZIKV) infection and pathogenesis are linked to the disruption of neurogenesis, congenital Zika syndrome and microcephaly by affecting neural progenitor cells. Nonstructural protein 5 (NS5) is the largest product encoded by ZIKV-RNA and is important for replication and immune evasion. Here, we studied the potential effects of NS5 on microtubules (MTs) and autophagy flux, together with the interplay of NS5 with histone deacetylase 6 (HDAC6). Fluorescence microscopy, biochemical cell-fractionation combined with the use of HDAC6 mutants, chemical inhibitors and RNA interference indicated that NS5 accumulates in nuclear structures and strongly promotes the acetylation of MTs that aberrantly reorganize in nested structures. Similarly, NS5 accumulates the p62 protein, an autophagic-flux marker. Therefore, NS5 alters events that are under the control of the autophagic tubulin-deacetylase HDAC6. HDAC6 appears to degrade NS5 by autophagy in a deacetylase- and BUZ domain-dependent manner and to control the cytoplasmic expression of NS5. Moreover, NS5 inhibits RNA-mediated RIG-I interferon (IFN) production, resulting in greater activity when autophagy is inhibited (i.e., effect correlated with NS5 stability). Therefore, it is conceivable that NS5 contributes to cell toxicity and pathogenesis, evading the IFN-immune response by overcoming HDAC6 functions. HDAC6 has emerged as an anti-ZIKV factor by targeting NS5. Full article
(This article belongs to the Special Issue Untangling the Cross-Talk between Immune Responses and Infection)
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27 pages, 11107 KiB  
Article
Autologous T-Cell-Free Antigen Presentation System Unveils hCMV-Specific NK Cell Response
by Maria O. Ustiuzhanina, Maria A. Streltsova, Nikita D. Timofeev, Maxim A. Kryukov, Dmitriy M. Chudakov and Elena I. Kovalenko
Cells 2024, 13(6), 530; https://doi.org/10.3390/cells13060530 - 17 Mar 2024
Cited by 1 | Viewed by 1090
Abstract
NK cells play a decisive role in controlling hCMV infection by combining innate and adaptive-like immune reactions. The hCMV-derived VMAPRTLFL (LFL) peptide is a potent activator of NKG2C+ NK cells. Proposed here is an autologous system of LFL stimulation without T lymphocytes [...] Read more.
NK cells play a decisive role in controlling hCMV infection by combining innate and adaptive-like immune reactions. The hCMV-derived VMAPRTLFL (LFL) peptide is a potent activator of NKG2C+ NK cells. Proposed here is an autologous system of LFL stimulation without T lymphocytes and exogenous cytokines that allows us to evaluate NK-cell hCMV-specific responses in more native settings. In this model, we evaluated LFL-induced IFNγ production, focusing on signaling pathways and the degranulation and proliferation of NK cells orchestrated by microenvironment cytokine production and analyzed the transcriptome of expanded NK cells. NK cells of individuals having high anti-hCMV-IgG levels, in contrast to NK cells of hCMV-seronegative and low-positive donors, displayed increased IFNγ production and degranulation and activation levels and enhanced proliferation upon LFL stimulation. Cytokine profiles of these LFL-stimulated cultures demonstrated a proinflammatory shift. LFL-induced NK-cell IFNγ production was dependent on the PI3K and Ras/Raf/Mek signaling pathways, independently of cytokines. In hCMV-seropositive individuals, this model allowed obtaining NK-cell antigen-specific populations proliferating in response to LFL. The transcriptomic profile of these expanded NK cells showed increased adaptive gene expression and metabolic activation. The results complement the existing knowledge about hCMV-specific NK-cell response. This model may be further exploited for the identification and characterization of antigen-specific NK cells. Full article
(This article belongs to the Special Issue Untangling the Cross-Talk between Immune Responses and Infection)
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24 pages, 5080 KiB  
Article
Differential Activation of Splenic cDC1 and cDC2 Cell Subsets following Poxvirus Infection of BALB/c and C57BL/6 Mice
by Lidia Szulc-Dąbrowska, Zuzanna Biernacka, Michał Koper, Justyna Struzik, Małgorzata Gieryńska, Ada Schollenberger, Iwona Lasocka and Felix N. Toka
Cells 2024, 13(1), 13; https://doi.org/10.3390/cells13010013 - 20 Dec 2023
Cited by 1 | Viewed by 1188
Abstract
Conventional dendritic cells (cDCs) are innate immune cells that play a pivotal role in inducing antiviral adaptive immune responses due to their extraordinary ability to prime and polarize naïve T cells into different effector T helper (Th) subsets. The two major subpopulations of [...] Read more.
Conventional dendritic cells (cDCs) are innate immune cells that play a pivotal role in inducing antiviral adaptive immune responses due to their extraordinary ability to prime and polarize naïve T cells into different effector T helper (Th) subsets. The two major subpopulations of cDCs, cDC1 (CD8α+ in mice and CD141+ in human) and cDC2 (CD11b+ in mice and CD1c+ in human), can preferentially polarize T cells toward a Th1 and Th2 phenotype, respectively. During infection with ectromelia virus (ECTV), an orthopoxvirus from the Poxviridae family, the timing and activation of an appropriate Th immune response contributes to the resistance (Th1) or susceptibility (Th2) of inbred mouse strains to the lethal form of mousepox. Due to the high plasticity and diverse properties of cDC subpopulations in regulating the quality of a specific immune response, in the present study we compared the ability of splenic cDC1 and cDC2 originating from different ECTV-infected mouse strains to mature, activate, and polarize the Th immune response during mousepox. Our results demonstrated that during early stages of mousepox, both cDC subsets from resistant C57BL/6 and susceptible BALB/c mice were activated upon in vivo ECTV infection. These cells exhibited elevated levels of surface MHC class I and II, and co-stimulatory molecules and showed enhanced potential to produce cytokines. However, both cDC subsets from BALB/c mice displayed a higher maturation status than that of their counterparts from C57BL/6 mice. Despite their higher activation status, cDC1 and cDC2 from susceptible mice produced low amounts of Th1-polarizing cytokines, including IL-12 and IFN-γ, and the ability of these cells to stimulate the proliferation and Th1 polarization of allogeneic CD4+ T cells was severely compromised. In contrast, both cDC subsets from resistant mice produced significant amounts of Th1-polarizing cytokines and demonstrated greater capability in differentiating allogeneic T cells into Th1 cells compared to cDCs from BALB/c mice. Collectively, our results indicate that in the early stages of mousepox, splenic cDC subpopulations from the resistant mouse strain can better elicit a Th1 cell-mediated response than the susceptible strain can, probably contributing to the induction of the protective immune responses necessary for the control of virus dissemination and for survival from ECTV challenge. Full article
(This article belongs to the Special Issue Untangling the Cross-Talk between Immune Responses and Infection)
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