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  1. Artikel ; Online: Interaction of the antiphospholipid syndrome autoantigen beta-2 glycoprotein I with DNA and neutrophil extracellular traps.

    Kmeťová, Katarína / Lonina, Elena / Yalavarthi, Srilakshmi / Levine, Jerrold S / Hoy, Claire K / Sarosh, Cyrus / Gockman, Kelsey / Morris, Alexandra E / Tambralli, Ajay / Madison, Jacqueline A / Zuo, Yu / Subang, Rebecca / Rauch, Joyce / Knight, Jason S

    Clinical immunology (Orlando, Fla.)

    2023  Band 255, Seite(n) 109714

    Abstract: Beta-2 glycoprotein I ( ... ...

    Abstract Beta-2 glycoprotein I (β
    Sprache Englisch
    Erscheinungsdatum 2023-07-30
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 1459903-x
    ISSN 1521-7035 ; 1521-6616
    ISSN (online) 1521-7035
    ISSN 1521-6616
    DOI 10.1016/j.clim.2023.109714
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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  2. Artikel ; Online: Release of neutrophil extracellular traps by neutrophils stimulated with antiphospholipid antibodies: a newly identified mechanism of thrombosis in the antiphospholipid syndrome.

    Yalavarthi, Srilakshmi / Gould, Travis J / Rao, Ashish N / Mazza, Levi F / Morris, Alexandra E / Núñez-Álvarez, Carlos / Hernández-Ramírez, Diego / Bockenstedt, Paula L / Liaw, Patricia C / Cabral, Antonio R / Knight, Jason S

    Arthritis & rheumatology (Hoboken, N.J.)

    2015  Band 67, Heft 11, Seite(n) 2990–3003

    Abstract: Objective: Antiphospholipid antibodies (aPL), especially those targeting β2 -glycoprotein I (β2 GPI), are well known to activate endothelial cells, monocytes, and platelets, with prothrombotic implications. In contrast, the interaction of aPL with ... ...

    Abstract Objective: Antiphospholipid antibodies (aPL), especially those targeting β2 -glycoprotein I (β2 GPI), are well known to activate endothelial cells, monocytes, and platelets, with prothrombotic implications. In contrast, the interaction of aPL with neutrophils has not been extensively studied. Neutrophil extracellular traps (NETs) have recently been recognized as an important activator of the coagulation cascade, as well as an integral component of arterial and venous thrombi. This study was undertaken to determine whether aPL activate neutrophils to release NETs, thereby predisposing to the arterial and venous thrombosis inherent in the antiphospholipid syndrome (APS).
    Methods: Neutrophils, sera, and plasma were prepared from patients with primary APS (n = 52) or from healthy volunteers and characterized. No patient had concomitant systemic lupus erythematosus.
    Results: Sera and plasma from patients with primary APS had elevated levels of both cell-free DNA and NETs, as compared to healthy volunteers. Freshly isolated neutrophils from patients with APS were predisposed to high levels of spontaneous NET release. Further, APS patient sera, as well as IgG purified from APS patients, stimulated NET release from control neutrophils. Human aPL monoclonal antibodies, especially those targeting β2 GPI, also enhanced NET release. The induction of APS NETs was abrogated with inhibitors of reactive oxygen species formation and Toll-like receptor 4 signaling. Highlighting the potential clinical relevance of these findings, APS NETs promoted thrombin generation.
    Conclusion: Our findings indicate that NET release warrants further investigation as a novel therapeutic target in APS.
    Mesh-Begriff(e) Antibodies, Antiphospholipid/immunology ; Antiphospholipid Syndrome/immunology ; Antiphospholipid Syndrome/metabolism ; Extracellular Traps ; Humans ; Immunoglobulin G/immunology ; Neutrophils/immunology ; Neutrophils/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction/physiology ; Thrombosis/immunology ; Thrombosis/metabolism ; Toll-Like Receptor 4/metabolism
    Chemische Substanzen Antibodies, Antiphospholipid ; Immunoglobulin G ; Reactive Oxygen Species ; TLR4 protein, human ; Toll-Like Receptor 4
    Sprache Englisch
    Erscheinungsdatum 2015-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.39247
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

    Zusatzmaterialien

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 24: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

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