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dc.contributor.authorRekvig, Ole Petter
dc.date.accessioned2025-03-11T09:58:16Z
dc.date.available2025-03-11T09:58:16Z
dc.date.issued2025-01-28
dc.description.abstractn attempts to understand systemic lupus erythematosus (SLE), we find ourselves in the intellectual cross-point between nosology, pathogenicity-oriented science, philosophy, empiricism, and qualified conjectures. A vital consequence in science theory is that scientific hypotheses that are not critically investigated are in danger of being transformed into scientific dogmas. This statement has consequences for this study. Two central problematic aspects are discussed. For the first, we have to consider new selection principles for classification criteria—implying integration of the causality principle. Second, central historical data must be implemented if we aim to understand SLE. These data comprise famous descriptions of distinct, dynamically changing DNA structures linked to the genetic machinery. These unique structures have since their discoveries decades ago mostly been ignored in SLE research. Likewise, inconclusive dogmatic data indicate that different glomerular ligands are recognized by nephritogenic anti-dsDNA antibodies—exposed chromatin fragments or inherent membrane ligands. These incongruent models have not been comparatively and systematically investigated. Three research areas will be critically discussed: (i) selection and role of SLE classification criteria, a process that must imply the causality principle; (ii) definition and impact of anti-dsDNA structure-specific antibodies; (iii) incongruent pathogenic models that account for lupus nephritis. A precise and critically important question is if SLE itself is a response to a dominant unified cause that initiates a cascade of downstream effects (criteria) or if SLE represents combined responses to a random interplay of multiple cause-effect events. These principally different explanations are formally not excluded or accepted today. Currently, SLE may be regarded as a disease with phenotypic diversity, independently segregated manifestations with unresolved etiologies that are not unique to a single SLE phenotype. The focus for the present discussion is basically how we, by critical hypotheses, can re-consider science-based selection of SLE classification criteria in order to delimitate and rationalize SLE. Classification criteria, autoimmunity, DNA structures, and anti-dsDNA antibodies are integrated aspects in this discussion.en_US
dc.identifier.citationRekvig. Why is it so difficult to understand why we don’t understand human systemic lupus erythematosus? Contemplating facts, conflicts, and impact of “the causality cascade paradigm”. Frontiers in Immunology. 2024;15en_US
dc.identifier.cristinIDFRIDAID 2364881
dc.identifier.doi10.3389/fimmu.2024.1507792
dc.identifier.issn1664-3224
dc.identifier.urihttps://hdl.handle.net/10037/36659
dc.language.isoengen_US
dc.publisherFrontiers Mediaen_US
dc.relation.journalFrontiers in Immunology
dc.rights.accessRightsopenAccessen_US
dc.rights.holderCopyright 2024 The Author(s)en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0en_US
dc.rightsAttribution 4.0 International (CC BY 4.0)en_US
dc.titleWhy is it so difficult to understand why we don’t understand human systemic lupus erythematosus? Contemplating facts, conflicts, and impact of “the causality cascade paradigm”en_US
dc.type.versionpublishedVersionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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Attribution 4.0 International (CC BY 4.0)
Med mindre det står noe annet, er denne innførselens lisens beskrevet som Attribution 4.0 International (CC BY 4.0)