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dc.contributor.authorRekvig, Ole Petter
dc.date.accessioned2019-10-16T13:22:35Z
dc.date.available2019-10-16T13:22:35Z
dc.date.issued2019-05-15
dc.description.abstractThis study aims to understand what lupus nephritis is, its origin, clinical context, and its pathogenesis. Truly, we encounter many conceptual and immanent tribulations in our attempts to search for the pathogenesis of this disease—and how to explain its assumed link to SLE. Central in the present landscape stay a short history of the early studies that substantiated the structures of isolated or chromatin-assembled mammalian dsDNA, and its assumed, highly controversial role in induction of anti-dsDNA antibodies. Arguments discussed here may provoke the view that anti-dsDNA antibodies are not what we think they are, as they may be antibodies operational in quite different biological contexts, although they bind dsDNA by chance. This may not mean that these antibodies are not pathogenic but they do not inform how they are so. This theoretical study centers the content around the origin and impact of extra-cellular DNA, and if dsDNA has an effect on the adaptive immune system. The pathogenic potential of chromatin-anti-dsDNA antibody interactions is limited to incite lupus nephritis and dermatitis which may be linked in a common pathogenic process. These are major criteria in SLE classification systems but are not shared with other defined manifestations in SLE, which may mean that they are their own disease entities, and not integrated in SLE. Today, the models thought to explain lupus nephritis are divergent and inconsistent. We miss a comprehensive perspective to try the different models against each other. To do this, we need to take all elements of the syndrome SLE into account. This can only be achieved by concentrating on the interactions between autoimmunity, immunopathology, deviant cell death and necrotic chromatin in context of elements of system science. System science provides a framework where data generated by experts can be compared, and tested against each other. This approach open for consensus on central elements making up “lupus nephritis” to separate what we agree on and how to understand the basis for conflicting models. This has not been done yet in a systematic context.en_US
dc.descriptionSource at <a href=https://doi.org/10.3389/fimmu.2019.01104>https://doi.org/10.3389/fimmu.2019.01104. </a>en_US
dc.identifier.citationRekvig, O.P. (2019). The dsDNA, Anti-dsDNA Antibody, and Lupus Nephritis: What We Agree on, What Must Be Done, and What the Best Strategy Forward Could Be. <i>Frontiers in Immunology, 10</i>:1104. https://doi.org/10.3389/fimmu.2019.01104en_US
dc.identifier.cristinIDFRIDAID 1712480
dc.identifier.doi10.3389/fimmu.2019.01104
dc.identifier.issn1664-3224
dc.identifier.urihttps://hdl.handle.net/10037/16420
dc.language.isoengen_US
dc.publisherFrontiers Mediaen_US
dc.relation.journalFrontiers in Immunology
dc.rights.accessRightsopenAccessen_US
dc.subjectVDP::Medical disciplines: 700::Basic medical, dental and veterinary science disciplines: 710en_US
dc.subjectVDP::Medisinske Fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710en_US
dc.subjectchromatinen_US
dc.subjectdsDNAen_US
dc.subjectautoimmunityen_US
dc.subjectlupus nephritisen_US
dc.subjectenigmaen_US
dc.subjectcontroversiesen_US
dc.titleThe dsDNA, Anti-dsDNA Antibody, and Lupus Nephritis: What We Agree on, What Must Be Done, and What the Best Strategy Forward Could Been_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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