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  1. Article ; Online: Development and preclinical evaluation of virus-like particle vaccine against COVID-19 infection.

    Yilmaz, Ismail Cem / Ipekoglu, Emre Mert / Bulbul, Artun / Turay, Nilsu / Yildirim, Muzaffer / Evcili, Irem / Yilmaz, Naz Surucu / Guvencli, Nese / Aydin, Yagmur / Gungor, Bilgi / Saraydar, Berfu / Bartan, Asli Gulce / Ibibik, Bilgehan / Bildik, Tugce / Baydemir, İlayda / Sanli, Hatice Asena / Kayaoglu, Basak / Ceylan, Yasemin / Yildirim, Tugce /
    Abras, Irem / Ayanoglu, Ihsan Cihan / Cam, Sefa Burak / Ciftci Dede, Eda / Gizer, Merve / Erganis, Osman / Sarac, Fahriye / Uzar, Serdar / Enul, Hakan / Adiay, Cumhur / Aykut, Gamze / Polat, Hivda / Yildirim, Ismail Selim / Tekin, Saban / Korukluoglu, Gulay / Zeytin, Hasan Ersin / Korkusuz, Petek / Gursel, Ihsan / Gursel, Mayda

    Allergy

    2021  Volume 77, Issue 1, Page(s) 258–270

    Abstract: Background: Vaccines that incorporate multiple SARS-CoV-2 antigens can further broaden the breadth of virus-specific cellular and humoral immunity. This study describes the development and immunogenicity of SARS-CoV-2 VLP vaccine that incorporates the ... ...

    Abstract Background: Vaccines that incorporate multiple SARS-CoV-2 antigens can further broaden the breadth of virus-specific cellular and humoral immunity. This study describes the development and immunogenicity of SARS-CoV-2 VLP vaccine that incorporates the four structural proteins of SARS-CoV-2.
    Methods: VLPs were generated in transiently transfected HEK293 cells, purified by multimodal chromatography, and characterized by tunable-resistive pulse sensing, AFM, SEM, and TEM. Immunoblotting studies verified the protein identities of VLPs. Cellular and humoral immune responses of immunized animals demonstrated the immune potency of the formulated VLP vaccine.
    Results: Transiently transfected HEK293 cells reproducibly generated vesicular VLPs that were similar in size to and expressing all four structural proteins of SARS-CoV-2. Alum adsorbed, K3-CpG ODN-adjuvanted VLPs elicited high titer anti-S, anti-RBD, anti-N IgG, triggered multifunctional Th1-biased T-cell responses, reduced virus load, and prevented lung pathology upon live virus challenge in vaccinated animals.
    Conclusion: These data suggest that VLPs expressing all four structural protein antigens of SARS-CoV-2 are immunogenic and can protect animals from developing COVID-19 infection following vaccination.
    MeSH term(s) Animals ; Antibodies, Neutralizing ; Antibodies, Viral ; COVID-19 ; COVID-19 Vaccines ; HEK293 Cells ; Humans ; SARS-CoV-2 ; Vaccines, Virus-Like Particle
    Chemical Substances Antibodies, Neutralizing ; Antibodies, Viral ; COVID-19 Vaccines ; Vaccines, Virus-Like Particle
    Language English
    Publishing date 2021-09-21
    Publishing country Denmark
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 391933-x
    ISSN 1398-9995 ; 0105-4538
    ISSN (online) 1398-9995
    ISSN 0105-4538
    DOI 10.1111/all.15091
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Type I IFN-related NETosis in ataxia telangiectasia and Artemis deficiency.

    Gul, Ersin / Sayar, Esra Hazar / Gungor, Bilgi / Eroglu, Fehime Kara / Surucu, Naz / Keles, Sevgi / Guner, Sukru Nail / Findik, Siddika / Alpdundar, Esin / Ayanoglu, Ihsan Cihan / Kayaoglu, Basak / Geckin, Busra Nur / Sanli, Hatice Asena / Kahraman, Tamer / Yakicier, Cengiz / Muftuoglu, Meltem / Oguz, Berna / Cagdas Ayvaz, Deniz Nazire / Gursel, Ihsan /
    Ozen, Seza / Reisli, Ismail / Gursel, Mayda

    The Journal of allergy and clinical immunology

    2017  Volume 142, Issue 1, Page(s) 246–257

    Abstract: Background: Pathological inflammatory syndromes of unknown etiology are commonly observed in ataxia telangiectasia (AT) and Artemis deficiency. Similar inflammatory manifestations also exist in patients with STING-associated vasculopathy in infancy ( ... ...

    Abstract Background: Pathological inflammatory syndromes of unknown etiology are commonly observed in ataxia telangiectasia (AT) and Artemis deficiency. Similar inflammatory manifestations also exist in patients with STING-associated vasculopathy in infancy (SAVI).
    Objective: We sought to test the hypothesis that the inflammation-associated manifestations observed in patients with AT and Artemis deficiency stem from increased type I IFN signature leading to neutrophil-mediated pathological damage.
    Methods: Cytokine/protein signatures were determined by ELISA, cytometric bead array, or quantitative PCR. Stat1 phosphorylation levels were determined by flow cytometry. DNA species accumulating in the cytosol of patients' cells were quantified microscopically and flow cytometrically. Propensity of isolated polymorhonuclear granulocytes to form neutrophil extracellular traps (NETs) was determined using fluorescence microscopy and picogreen assay. Neutrophil reactive oxygen species levels and mitochondrial stress were assayed using fluorogenic probes, microscopy, and flow cytometry.
    Results: Type I and III IFN signatures were elevated in plasma and peripheral blood cells of patients with AT, Artemis deficiency, and SAVI. Chronic IFN production stemmed from the accumulation of DNA in the cytoplasm of AT and Artemis-deficient cells. Neutrophils isolated from patients spontaneously produced NETs and displayed indicators of oxidative and mitochondrial stress, supportive of their NETotic tendencies. A similar phenomenon was also observed in neutrophils from healthy controls exposed to patient plasma samples or exogeneous IFN-α.
    Conclusions: Type I IFN-mediated neutrophil activation and NET formation may contribute to inflammatory manifestations observed in patients with AT, Artemis deficiency, and SAVI. Thus, neutrophils represent a promising target to manage inflammatory syndromes in diseases with active type I IFN signature.
    MeSH term(s) Ataxia Telangiectasia/immunology ; Ataxia Telangiectasia/pathology ; DNA-Binding Proteins ; Endonucleases/deficiency ; Endonucleases/immunology ; Extracellular Traps/immunology ; Humans ; Immunologic Deficiency Syndromes/genetics ; Immunologic Deficiency Syndromes/immunology ; Interferon Type I/immunology ; Membrane Proteins/genetics ; Neutrophil Activation ; Neutrophils/immunology ; Neutrophils/pathology ; Nuclear Proteins/deficiency ; Nuclear Proteins/immunology ; Vasculitis/genetics ; Vasculitis/immunology ; Vasculitis/pathology
    Chemical Substances DNA-Binding Proteins ; Interferon Type I ; Membrane Proteins ; Nuclear Proteins ; STING1 protein, human ; DCLRE1C protein, human (EC 3.1.-) ; Endonucleases (EC 3.1.-)
    Language English
    Publishing date 2017-11-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2017.10.030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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