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  1. Article ; Online: Casting a Wide NET.

    Kaplan, Mariana J

    Journal of immunology (Baltimore, Md. : 1950)

    2022  Volume 209, Issue 5, Page(s) 843–844

    Language English
    Publishing date 2022-08-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural
    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.2200173
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Mitochondria shape neutrophils during hypoxia.

    Kaplan, Mariana J

    Blood

    2022  Volume 139, Issue 2, Page(s) 159–160

    MeSH term(s) Humans ; Hypoxia/metabolism ; Mitochondria ; Neutrophils/metabolism
    Language English
    Publishing date 2022-01-13
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2021013440
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  3. Article ; Online: Mitochondrial dysfunction in the erythroid compartment.

    Kaplan, Mariana J

    Nature immunology

    2021  Volume 22, Issue 11, Page(s) 1354–1355

    MeSH term(s) Erythroid Cells/metabolism ; Mitochondria
    Language English
    Publishing date 2021-10-19
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-021-01050-9
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  4. Article ; Online: Vascular damage in systemic lupus erythematosus.

    Ambler, William G / Kaplan, Mariana J

    Nature reviews. Nephrology

    2024  Volume 20, Issue 4, Page(s) 251–265

    Abstract: Vascular disease is a major cause of morbidity and mortality in patients with systemic autoimmune diseases, particularly systemic lupus erythematosus (SLE). Although comorbid cardiovascular risk factors are frequently present in patients with SLE, they ... ...

    Abstract Vascular disease is a major cause of morbidity and mortality in patients with systemic autoimmune diseases, particularly systemic lupus erythematosus (SLE). Although comorbid cardiovascular risk factors are frequently present in patients with SLE, they do not explain the high burden of premature vascular disease. Profound innate and adaptive immune dysregulation seems to be the primary driver of accelerated vascular damage in SLE. In particular, evidence suggests that dysregulation of type 1 interferon (IFN-I) and aberrant neutrophils have key roles in the pathogenesis of vascular damage. IFN-I promotes endothelial dysfunction directly via effects on endothelial cells and indirectly via priming of immune cells that contribute to vascular damage. SLE neutrophils are vasculopathic in part because of their increased ability to form immunostimulatory neutrophil extracellular traps. Despite improvements in clinical care, cardiovascular disease remains the leading cause of mortality among patients with SLE, and treatments that improve vascular outcomes are urgently needed. Improved understanding of the mechanisms of vascular injury in inflammatory conditions such as SLE could also have implications for common cardiovascular diseases, such as atherosclerosis and hypertension, and may ultimately lead to personalized therapeutic approaches to the prevention and treatment of this potentially fatal complication.
    MeSH term(s) Humans ; Endothelial Cells/pathology ; Lupus Erythematosus, Systemic/complications ; Lupus Erythematosus, Systemic/pathology ; Neutrophils ; Extracellular Traps ; Atherosclerosis/etiology ; Cardiovascular Diseases/etiology ; Interferon Type I
    Chemical Substances Interferon Type I
    Language English
    Publishing date 2024-01-03
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/s41581-023-00797-8
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  5. Article ; Online: Linking clotting and autoimmunity.

    Kaplan, Mariana J

    Science (New York, N.Y.)

    2021  Volume 371, Issue 6534, Page(s) 1100–1101

    MeSH term(s) Autoimmunity ; Blood Coagulation ; Endothelial Protein C Receptor ; Lipids
    Chemical Substances Endothelial Protein C Receptor ; Lipids
    Language English
    Publishing date 2021-03-11
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.abg6449
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  6. Article ; Online: Targeting the Myddosome in Systemic Autoimmunity: Ready for Prime Time?

    Kaplan, Mariana J

    Arthritis & rheumatology (Hoboken, N.J.)

    2021  Volume 73, Issue 12, Page(s) 2163–2165

    MeSH term(s) Autoimmunity ; Interleukin-1 Receptor-Associated Kinases ; Myeloid Differentiation Factor 88
    Chemical Substances Myeloid Differentiation Factor 88 ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2021-11-02
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.41951
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  7. Article ; Online: Reply.

    Blanco, Luz P / Kaplan, Mariana J

    Arthritis & rheumatology (Hoboken, N.J.)

    2022  Volume 75, Issue 1, Page(s) 143–144

    Language English
    Publishing date 2022-12-01
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.42328
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  8. Article ; Online: Of larks and owls.

    Kaplan, Mariana J

    Nature immunology

    2020  Volume 21, Issue 2, Page(s) 104–105

    MeSH term(s) Animals ; Inflammation ; Neutrophils ; Passeriformes ; Proteome
    Chemical Substances Proteome
    Language English
    Publishing date 2020-01-13
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-019-0579-7
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  9. Article ; Online: "Rounding Third Base and Heading Home": Arthritis & Rheumatology in 2024.

    Solomon, Daniel H / Kaplan, Mariana J / Nigrovic, Peter A / Bucala, Richard

    Arthritis & rheumatology (Hoboken, N.J.)

    2024  

    Language English
    Publishing date 2024-04-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.42828
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  10. Book ; Online: NETosis 2: The Excitement Continues

    Herrmann, Martin / Radic, Marko / Kaplan, Mariana J.

    2017  

    Abstract: NETosis, a form of cell death that manifests by the release of decondensed chromatin to the extracellular space, provides valuable insights into mechanisms and consequences of cellular demise. Because extracellular chromatin can immobilize microbes, the ... ...

    Abstract NETosis, a form of cell death that manifests by the release of decondensed chromatin to the extracellular space, provides valuable insights into mechanisms and consequences of cellular demise. Because extracellular chromatin can immobilize microbes, the extended nucleohistone network was called a neutrophil extracellular trap (NET), and the process of chromatin release was proposed to serve an innate immune defense function. Extracellular chromatin NETs were initially observed in studies of neutrophils and are most prominent in these types of granulocytes. Subsequent studies showed that other granulocytes and, in a limited way, other cells of the innate immune response may also release nuclear chromatin following certain kinds of stimulation. Variations of NETosis were noted with cells that remain temporarily motile after the release of chromatin.-

    Numerous stimuli for NETosis were discovered, including bacterial breakdown products, inflammatory stimuli, particulate matter, certain crystals, immune complexes and activated thrombocytes. Fundamental explorations into the mechanisms of NETosis observed that neutrophil enzyme activity (PAD4, neutrophil elastase, proteinase 3 and myeloperoxidase) and signal transduction pathways contribute to the regulation of NETosis. Histones in NET chromatin become modified by peptidylarginine deiminase 4 (PAD4) and cleaved at specific sites by proteases, leading to extensive chromatin externalization. In addition, NETs serve for attachment of bactericidal enzymes including myeloperoxidase, leukocyte proteases, and the cathelicidin LL-37. NETs are decorated with proteases and may thus contribute to tissue destruction. However, the attachment of these enzymes to NET-associated supramolecular structures restricts systemic spread of the proteolytic activity.-

    While the benefit of NETs in an infection appears obvious, NETs also participate as key protagonists in various pathologic states. Therefore, it is essential for NETs to be efficiently cleared; otherwise digestive enzymes may gain access to tissues where inflammation takes place. Persistent NET exposure at sites of inflammation may lead to a further complication: NET antigens may provoke acquired immune responses and, over time, could initiate autoimmune reactions, serve as antigen for nuclear autoantibodies and foster DNA immune complex-related inflammation. Neutrophil products and deiminated proteins comprise an important group of autoantigens in musculoskeletal disorders. Aberrant NET synthesis and/or clearance are often associated with inflammatory and autoimmune conditions. Recent evidence also implicates aberrant NET formation in the development of endothelial damage, atherosclerosis and thrombosis.-
    Keywords Medicine (General) ; Immunologic diseases. Allergy
    Size 1 electronic resource (362 p.)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT020099575
    ISBN 9782889453795 ; 2889453790
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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