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  1. Article ; Online: Early production of IL-17A by γδ T cells in the trachea promotes viral clearance during influenza infection in mice.

    Palomino-Segura, Miguel / Latino, Irene / Farsakoglu, Yagmur / Gonzalez, Santiago F

    European journal of immunology

    2019  Volume 50, Issue 1, Page(s) 97–109

    Abstract: The innate immune response generated against influenza infection is critical for the inhibition of viral dissemination. The trachea contains different types of innate immune cells that protect the respiratory tract from pathogen invasion. Among them, γδ ... ...

    Abstract The innate immune response generated against influenza infection is critical for the inhibition of viral dissemination. The trachea contains different types of innate immune cells that protect the respiratory tract from pathogen invasion. Among them, γδ T cells have the ability to rapidly generate large amounts of pro-inflammatory cytokines to preserve mucosal barrier homeostasis during infection. However, little is known about their role during the early phase of influenza infection in the airways. In this study, we found that, early after infection, γδ T cells are recruited and activated in the trachea and outnumber αβ T cells during the course of the influenza infection that follows. We also showed that the majority of the recruited γδ T cells express the Vγ4 TCR chain and infiltrate in a process that involves the chemokine receptor CXCR3. In addition, we demonstrated that γδ T cells promote the recruitment of protective neutrophils and NK cells to the tracheal mucosa. Altogether, our results highlight the importance of the immune responses mediated by γδ T cells.
    MeSH term(s) Animals ; Immunity, Innate/immunology ; Interleukin-17/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Orthomyxoviridae Infections/immunology ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; T-Lymphocyte Subsets/immunology ; Trachea/immunology ; Trachea/virology
    Chemical Substances Il17a protein, mouse ; Interleukin-17 ; Receptors, Antigen, T-Cell, gamma-delta
    Language English
    Publishing date 2019-12-04
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.201948157
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Characterization of the Dynamic Behavior of Neutrophils Following Influenza Vaccination.

    Pizzagalli, Diego Ulisse / Latino, Irene / Pulfer, Alain / Palomino-Segura, Miguel / Virgilio, Tommaso / Farsakoglu, Yagmur / Krause, Rolf / Gonzalez, Santiago F

    Frontiers in immunology

    2019  Volume 10, Page(s) 2621

    Abstract: Neutrophils are amongst the first cells to respond to inflammation and infection. Although they play a key role in limiting the dissemination of pathogens, the study of their dynamic behavior in immune organs remains elusive. In this work, we ... ...

    Abstract Neutrophils are amongst the first cells to respond to inflammation and infection. Although they play a key role in limiting the dissemination of pathogens, the study of their dynamic behavior in immune organs remains elusive. In this work, we characterized
    MeSH term(s) Animals ; Chemokine CXCL1/physiology ; Influenza Vaccines/immunology ; Interleukin-1alpha/physiology ; Lymph Nodes/immunology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Neutrophils/immunology ; Phagocytosis ; Vaccination
    Chemical Substances Chemokine CXCL1 ; Cxcl1 protein, mouse ; Influenza Vaccines ; Interleukin-1alpha
    Language English
    Publishing date 2019-11-20
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2019.02621
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Plitidepsin as an Immunomodulator against Respiratory Viral Infections.

    Losada, Alejandro / Izquierdo-Useros, Nuria / Aviles, Pablo / Vergara-Alert, Júlia / Latino, Irene / Segalés, Joaquim / Gonzalez, Santiago F / Cuevas, Carmen / Raïch-Regué, Dàlia / Muñoz-Alonso, María J / Perez-Zsolt, Daniel / Muñoz-Basagoiti, Jordana / Rodon, Jordi / Chang, Lauren A / Warang, Prajakta / Singh, Gagandeep / Brustolin, Marco / Cantero, Guillermo / Roca, Núria /
    Pérez, Mònica / Bustos-Morán, Eugenio / White, Kris / Schotsaert, Michael / García-Sastre, Adolfo

    Journal of immunology (Baltimore, Md. : 1950)

    2024  Volume 212, Issue 8, Page(s) 1307–1318

    Abstract: Plitidepsin is a host-targeted compound known for inducing a strong anti-SARS-CoV-2 activity, as well as for having the capacity of reducing lung inflammation. Because IL-6 is one of the main cytokines involved in acute respiratory distress syndrome, the ...

    Abstract Plitidepsin is a host-targeted compound known for inducing a strong anti-SARS-CoV-2 activity, as well as for having the capacity of reducing lung inflammation. Because IL-6 is one of the main cytokines involved in acute respiratory distress syndrome, the effect of plitidepsin in IL-6 secretion in different in vitro and in vivo experimental models was studied. A strong plitidepsin-mediated reduction of IL-6 was found in human monocyte-derived macrophages exposed to nonproductive SARS-CoV-2. In resiquimod (a ligand of TLR7/8)-stimulated THP1 human monocytes, plitidepsin-mediated reductions of IL-6 mRNA and IL-6 levels were also noticed. Additionally, although resiquimod-induced binding to DNA of NF-κB family members was unaffected by plitidepsin, a decrease in the regulated transcription by NF-κB (a key transcription factor involved in the inflammatory cascade) was observed. Furthermore, the phosphorylation of p65 that is required for full transcriptional NF-κB activity was significantly reduced by plitidepsin. Moreover, decreases of IL-6 levels and other proinflammatory cytokines were also seen in either SARS-CoV-2 or H1N1 influenza virus-infected mice, which were treated at low enough plitidepsin doses to not induce antiviral effects. In summary, plitidepsin is a promising therapeutic agent for the treatment of viral infections, not only because of its host-targeted antiviral effect, but also for its immunomodulatory effect, both of which were evidenced in vitro and in vivo by the decrease of proinflammatory cytokines.
    MeSH term(s) Humans ; Animals ; Mice ; NF-kappa B/metabolism ; Influenza A Virus, H1N1 Subtype ; Interleukin-6/pharmacology ; Antiviral Agents/pharmacology ; Immunologic Factors/pharmacology ; Cytokines/metabolism ; SARS-CoV-2/metabolism ; Depsipeptides
    Chemical Substances NF-kappa B ; plitidepsin (Y76ID234HW) ; Interleukin-6 ; Antiviral Agents ; Immunologic Factors ; Cytokines ; Depsipeptides
    Language English
    Publishing date 2024-02-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.2300426
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Subcapsular Sinus Macrophages Promote Melanoma Metastasis to the Sentinel Lymph Nodes via an IL1α-STAT3 Axis.

    Virgilio, Tommaso / Bordini, Joy / Cascione, Luciano / Sartori, Giulio / Latino, Irene / Molina Romero, Daniel / Leoni, Cristina / Akhmedov, Murodzhon / Rinaldi, Andrea / Arribas, Alberto J / Morone, Diego / Seyed Jafari, S Morteza / Bersudsky, Marina / Ottolenghi, Aner / Kwee, Ivo / Chiaravalli, Anna Maria / Sessa, Fausto / Hunger, Robert E / Bruno, Antonino /
    Mortara, Lorenzo / Voronov, Elena / Monticelli, Silvia / Apte, Ron N / Bertoni, Francesco / Gonzalez, Santiago F

    Cancer immunology research

    2022  Volume 10, Issue 12, Page(s) 1525–1541

    Abstract: During melanoma metastasis, tumor cells originating in the skin migrate via lymphatic vessels to the sentinel lymph node (sLN). This process facilitates tumor cell spread across the body. Here, we characterized the innate inflammatory response to ... ...

    Abstract During melanoma metastasis, tumor cells originating in the skin migrate via lymphatic vessels to the sentinel lymph node (sLN). This process facilitates tumor cell spread across the body. Here, we characterized the innate inflammatory response to melanoma in the metastatic microenvironment of the sLN. We found that macrophages located in the subcapsular sinus (SS) produced protumoral IL1α after recognition of tumoral antigens. Moreover, we confirmed that the elimination of LN macrophages or the administration of an IL1α-specific blocking antibody reduced metastatic spread. To understand the mechanism of action of IL1α in the context of the sLN microenvironment, we applied single-cell RNA sequencing to microdissected metastases obtained from animals treated with the IL1α-specific blocking antibody. Among the different pathways affected, we identified STAT3 as one of the main targets of IL1α signaling in metastatic tumor cells. Moreover, we found that the antitumoral effect of the anti-IL1α was not mediated by lymphocytes because Il1r1 knockout mice did not show significant differences in metastasis growth. Finally, we found a synergistic antimetastatic effect of the combination of IL1α blockade and STAT3 inhibition with stattic, highlighting a new immunotherapy approach to preventing melanoma metastasis.
    MeSH term(s) Animals ; Mice ; Sentinel Lymph Node Biopsy ; Sentinel Lymph Node/pathology ; Lymphatic Metastasis/pathology ; Melanoma/pathology ; Macrophages/metabolism ; Lymphatic Vessels/metabolism ; Lymphatic Vessels/pathology ; Lymph Nodes/pathology ; Skin Neoplasms/pathology ; Tumor Microenvironment
    Language English
    Publishing date 2022-10-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2732489-8
    ISSN 2326-6074 ; 2326-6066
    ISSN (online) 2326-6074
    ISSN 2326-6066
    DOI 10.1158/2326-6066.CIR-22-0225
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Influenza Vaccination Induces NK-Cell-Mediated Type-II IFN Response that Regulates Humoral Immunity in an IL-6-Dependent Manner.

    Farsakoglu, Yagmur / Palomino-Segura, Miguel / Latino, Irene / Zanaga, Silvia / Chatziandreou, Nikolaos / Pizzagalli, Diego Ulisse / Rinaldi, Andrea / Bolis, Marco / Sallusto, Federica / Stein, Jens V / Gonzalez, Santiago F

    Cell reports

    2019  Volume 26, Issue 9, Page(s) 2307–2315.e5

    Abstract: The role of natural killer (NK) cells in the immune response against vaccines is not fully understood. Here, we examine the function of infiltrated NK cells in the initiation of the inflammatory response triggered by inactivated influenza virus vaccine ... ...

    Abstract The role of natural killer (NK) cells in the immune response against vaccines is not fully understood. Here, we examine the function of infiltrated NK cells in the initiation of the inflammatory response triggered by inactivated influenza virus vaccine in the draining lymph node (LN). We observed that, following vaccination, NK cells are recruited to the interfollicular and medullary areas of the LN and become activated by type I interferons (IFNs) produced by LN macrophages. The activation of NK cells leads to their early production of IFNγ, which in turn regulates the recruitment of IL-6+ CD11b+ dendritic cells. Finally, we demonstrate that the interleukin-6 (IL-6)-mediated inflammation is important for the development of an effective humoral response against influenza virus in the draining LN.
    MeSH term(s) Animals ; Cells, Cultured ; Female ; Immunity, Humoral ; Inflammation/immunology ; Influenza Vaccines/immunology ; Interferon Type I/physiology ; Interferon-gamma/metabolism ; Interleukin-6/biosynthesis ; Interleukin-6/physiology ; Killer Cells, Natural/immunology ; Lymph Nodes/immunology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout
    Chemical Substances Influenza Vaccines ; Interferon Type I ; Interleukin-6 ; interleukin-6, mouse ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2019-02-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2019.01.104
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Protection against influenza infection requires early recognition by inflammatory dendritic cells through C-type lectin receptor SIGN-R1.

    Palomino-Segura, Miguel / Perez, Laurent / Farsakoglu, Yagmur / Virgilio, Tommaso / Latino, Irene / D'Antuono, Rocco / Chatziandreou, Nikolaos / Pizzagalli, Diego U / Wang, Guojun / García-Sastre, Adolfo / Sallusto, Federica / Carroll, Michael C / Neyrolles, Olivier / Gonzalez, Santiago F

    Nature microbiology

    2019  Volume 4, Issue 11, Page(s) 1930–1940

    Abstract: The early phase of influenza infection occurs in the upper respiratory tract and the trachea, but little is known about the initial events of virus recognition and control of viral dissemination by the immune system. Here, we report that inflammatory ... ...

    Abstract The early phase of influenza infection occurs in the upper respiratory tract and the trachea, but little is known about the initial events of virus recognition and control of viral dissemination by the immune system. Here, we report that inflammatory dendritic cells (IDCs) are recruited to the trachea shortly after influenza infection through type I interferon-mediated production of the chemokine CCL2. We further show that recruited IDCs express the C-type lectin receptor SIGN-R1, which mediates direct recognition of the virus by interacting with N-linked glycans present in glycoproteins of the virion envelope. Activation of IDCs via SIGN-R1 triggers the production of the chemokines CCL5, CXCL9 and CXCL10, which initiate the recruitment of protective natural killer (NK) cells in the infected trachea. In the absence of SIGN-R1, the recruitment and activation of NK cells is impaired, leading to uncontrolled viral proliferation. In sum, our results provide insight into the orchestration of the early cellular and molecular events involved in immune protection against influenza.
    MeSH term(s) Animals ; Cell Adhesion Molecules/metabolism ; Chemokines/metabolism ; Dendritic Cells/immunology ; Disease Models, Animal ; Dogs ; Influenza A virus/immunology ; Interferon Type I/metabolism ; Killer Cells, Natural ; Lectins, C-Type/metabolism ; Madin Darby Canine Kidney Cells ; Mice ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/virology ; Receptors, Cell Surface/metabolism ; Trachea/immunology ; Trachea/virology
    Chemical Substances Cell Adhesion Molecules ; Chemokines ; DC-specific ICAM-3 grabbing nonintegrin ; Interferon Type I ; Lectins, C-Type ; Receptors, Cell Surface
    Language English
    Publishing date 2019-07-29
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2058-5276
    ISSN (online) 2058-5276
    DOI 10.1038/s41564-019-0506-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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