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  1. Article ; Online: Aspirin meets cGAS.

    Elkon, Keith B

    Nature reviews. Rheumatology

    2019  Volume 15, Issue 5, Page(s) 254–255

    MeSH term(s) Acetylation ; Aspirin ; Autoimmunity ; DNA ; Nucleotidyltransferases
    Chemical Substances DNA (9007-49-2) ; Nucleotidyltransferases (EC 2.7.7.-) ; Aspirin (R16CO5Y76E)
    Language English
    Publishing date 2019-03-26
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2491532-4
    ISSN 1759-4804 ; 1759-4790
    ISSN (online) 1759-4804
    ISSN 1759-4790
    DOI 10.1038/s41584-019-0205-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book ; Online: Apoptosis and its relevance to autoimmunity

    Elkon, Keith B.

    discusses the major areas of apoptosis research

    2006  

    Author's details vol. ed.: Keith B. Elkon
    Language English
    Size VIII + 210 S.
    Publisher Karger
    Publishing place Basel
    Publishing country Switzerland
    Document type Book ; Online
    HBZ-ID TT050388030
    ISBN 978-3-318-01294-1 ; 3-318-01294-7
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

    Full text online

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  3. Book: Apoptosis and its relevance to autoimmunity

    Elkon, Keith B.

    2 tables

    (Current directions in autoimmunity ; 9)

    2006  

    Author's details vol. ed. Keith B. Elkon
    Series title Current directions in autoimmunity ; 9
    Collection
    Keywords Apoptosis / immunology ; Autoimmune Diseases / physiopathology ; Autoimmunity / physiology ; Receptors, Immunologic / physiology ; Apoptosis ; Autoimmunität
    Subject Apoptose ; Programmierter Zelltod
    Language English
    Size VII, 210 S. : Ill., graph. Darst., 245 mm x 175 mm
    Publisher Karger
    Publishing place Basel u.a.
    Publishing country Switzerland
    Document type Book
    HBZ-ID HT014611033
    ISBN 3-8055-8036-3 ; 978-3-8055-8036-6
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2006 A 421 order for loan Magazin

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  4. Article ; Online: Review: Cell Death, Nucleic Acids, and Immunity: Inflammation Beyond the Grave.

    Elkon, Keith B

    Arthritis & rheumatology (Hoboken, N.J.)

    2018  Volume 70, Issue 6, Page(s) 805–816

    Abstract: Cells of the innate immune system are rigged with sensors that detect nucleic acids derived from microbes, especially viruses. It has become clear that these same sensors that respond to nucleic acids derived from damaged cells or defective intracellular ...

    Abstract Cells of the innate immune system are rigged with sensors that detect nucleic acids derived from microbes, especially viruses. It has become clear that these same sensors that respond to nucleic acids derived from damaged cells or defective intracellular processing are implicated in triggering diseases such as lupus and arthritis. The ways in which cells die and the concomitant presence of proteins and peptides that allow nucleic acids to re-enter cells profoundly influence innate immune responses. In this review, we briefly discusses different types of programmed necrosis, such as pyroptosis, necroptosis, and NETosis, and explains how nucleic acids can engage intracellular receptors and stimulate inflammation. Host protective mechanisms that include compartmentalization of receptors and nucleases as well as the consequences of nuclease deficiencies are explored. In addition, proximal and distal targets in the nucleic acid stimulation of inflammation are discussed in terms of their potential amenability to therapy for the attenuation of innate immune activation and disease pathogenesis.
    MeSH term(s) Cell Death/immunology ; Humans ; Immunity, Innate/genetics ; Inflammation/genetics ; Nucleic Acids/immunology
    Chemical Substances Nucleic Acids
    Language English
    Publishing date 2018-04-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.40452
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Role of the cGAS-STING pathway in systemic and organ-specific diseases.

    Skopelja-Gardner, Sladjana / An, Jie / Elkon, Keith B

    Nature reviews. Nephrology

    2022  Volume 18, Issue 9, Page(s) 558–572

    Abstract: Cells are equipped with numerous sensors that recognize nucleic acids, which probably evolved for defence against viruses. Once triggered, these sensors stimulate the production of type I interferons and other cytokines that activate immune cells and ... ...

    Abstract Cells are equipped with numerous sensors that recognize nucleic acids, which probably evolved for defence against viruses. Once triggered, these sensors stimulate the production of type I interferons and other cytokines that activate immune cells and promote an antiviral state. The evolutionary conserved enzyme cyclic GMP-AMP synthase (cGAS) is one of the most recently identified DNA sensors. Upon ligand engagement, cGAS dimerizes and synthesizes the dinucleotide second messenger 2',3'-cyclic GMP-AMP (cGAMP), which binds to the endoplasmic reticulum protein stimulator of interferon genes (STING) with high affinity, thereby unleashing an inflammatory response. cGAS-binding DNA is not restricted by sequence and must only be >45 nucleotides in length; therefore, cGAS can also be stimulated by self genomic or mitochondrial DNA. This broad specificity probably explains why the cGAS-STING pathway has been implicated in a number of autoinflammatory, autoimmune and neurodegenerative diseases; this pathway might also be activated during acute and chronic kidney injury. Therapeutic manipulation of the cGAS-STING pathway, using synthetic cyclic dinucleotides or inhibitors of cGAMP metabolism, promises to enhance immune responses in cancer or viral infections. By contrast, inhibitors of cGAS or STING might be useful in diseases in which this pro-inflammatory pathway is chronically activated.
    MeSH term(s) DNA ; Humans ; Interferon Type I ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Nucleotidyltransferases/genetics ; Nucleotidyltransferases/metabolism ; Signal Transduction
    Chemical Substances Interferon Type I ; Membrane Proteins ; STING1 protein, human ; DNA (9007-49-2) ; Nucleotidyltransferases (EC 2.7.7.-) ; cGAS protein, human (EC 2.7.7.-)
    Language English
    Publishing date 2022-06-22
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/s41581-022-00589-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 107: Show issues

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  6. Article ; Online: The (Orf)ull truth about IRF5 and type I interferons in SLE.

    Elkon, Keith B / Briggs, Tracy A

    Nature reviews. Rheumatology

    2020  Volume 16, Issue 10, Page(s) 543–544

    MeSH term(s) Humans ; Interferon Regulatory Factors/genetics ; Interferon Regulatory Factors/metabolism ; Interferon Type I ; Lupus Erythematosus, Systemic ; Membrane Transport Proteins ; Nerve Tissue Proteins ; Toll-Like Receptor 7
    Chemical Substances IRF5 protein, human ; Interferon Regulatory Factors ; Interferon Type I ; Membrane Transport Proteins ; Nerve Tissue Proteins ; SLC15A4 protein, human ; TLR7 protein, human ; Toll-Like Receptor 7
    Language English
    Publishing date 2020-07-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2491532-4
    ISSN 1759-4804 ; 1759-4790
    ISSN (online) 1759-4804
    ISSN 1759-4790
    DOI 10.1038/s41584-020-0472-7
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  7. Article ; Online: B cell-activating factor (BAFF) from dendritic cells, monocytes and neutrophils is required for B cell maturation and autoantibody production in SLE-like autoimmune disease.

    Giordano, Daniela / Kuley, Runa / Draves, Kevin E / Elkon, Keith B / Giltiay, Natalia V / Clark, Edward A

    Frontiers in immunology

    2023  Volume 14, Page(s) 1050528

    Abstract: Purpose and methods: B cell-activating factor (BAFF) contributes to the pathogenesis of autoimmune diseases including systemic lupus erythematosus (SLE). Although several anti-BAFF Abs and derivatives have been developed for the treatment of SLE, the ... ...

    Abstract Purpose and methods: B cell-activating factor (BAFF) contributes to the pathogenesis of autoimmune diseases including systemic lupus erythematosus (SLE). Although several anti-BAFF Abs and derivatives have been developed for the treatment of SLE, the specific sources of BAFF that sustain autoantibody (auto-Ab) producing cells have not been definitively identified. Using BAFF-RFP reporter mice, we identified major changes in BAFF-producing cells in two mouse spontaneous lupus models (
    Results: First, we confirmed that similar to their wildtype
    Conclusions: Our findings underscore the importance of considering the relative roles of specific myeloid BAFF sources and B cell niches when developing treatments for SLE and other BAFF-associated autoimmune diseases.
    MeSH term(s) Animals ; Mice ; Autoantibodies ; Autoimmune Diseases/metabolism ; Dendritic Cells/metabolism ; Disease Models, Animal ; Interleukin-4/metabolism ; Lupus Erythematosus, Systemic ; Monocytes/metabolism ; Neutrophils ; Toll-Like Receptor 7/metabolism
    Chemical Substances Autoantibodies ; Interleukin-4 (207137-56-2) ; pristane (26HZV48DT1) ; Toll-Like Receptor 7 ; Tnfsf13b protein, mouse
    Language English
    Publishing date 2023-02-27
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1050528
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  8. Article ; Online: Poking holes in rheumatoid joints.

    Elkon, Keith B

    Science translational medicine

    2013  Volume 5, Issue 209, Page(s) 209fs39

    Abstract: Pathological mechanisms that cause cell membrane lysis and an increase in intracellular calcium may explain how rheumatoid arthritis patients develop citrullination of intracellular proteins in their joints (Romero et al., this issue). ...

    Abstract Pathological mechanisms that cause cell membrane lysis and an increase in intracellular calcium may explain how rheumatoid arthritis patients develop citrullination of intracellular proteins in their joints (Romero et al., this issue).
    MeSH term(s) Arthritis, Rheumatoid/immunology ; Arthritis, Rheumatoid/pathology ; Autoantigens/immunology ; Citrulline/metabolism ; Humans
    Chemical Substances Autoantigens ; Citrulline (29VT07BGDA)
    Language English
    Publishing date 2013-10-30
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.3007515
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6941: Show issues Location:
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  9. Book: Neurologic aspects of rheumatic diseases

    Elkon, Keith B.

    (Rheumatic disease clinics of North America ; 19,4)

    1993  

    Author's details Keith B. Elkon, guest ed
    Series title Rheumatic disease clinics of North America ; 19,4
    Collection
    Keywords Rheumatic Diseases / complications ; Nervous System Diseases / etiology ; Neurologic Manifestations
    Language English
    Size XII S., S. 765 - 1033 : Ill., graph. Darst.
    Publisher Saunders
    Publishing place Philadelphia u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT006147308
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    Se 363 -19,4- verfügbar in Königswinter Königswinter

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  10. Article ; Online: Autoimmunity: apoptotic fats grease transcription.

    Elkon, Keith B

    Nature medicine

    2009  Volume 15, Issue 11, Page(s) 1246–1248

    MeSH term(s) Animals ; Apoptosis/physiology ; Autoimmunity/physiology ; Lipids/physiology ; Liver X Receptors ; Orphan Nuclear Receptors/metabolism ; PPAR delta/genetics ; PPAR delta/metabolism ; Transcriptional Activation
    Chemical Substances Lipids ; Liver X Receptors ; Orphan Nuclear Receptors ; PPAR delta
    Language English
    Publishing date 2009-11-05
    Publishing country United States
    Document type News ; Comment
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/nm1109-1246
    Database MEDical Literature Analysis and Retrieval System OnLINE

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