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dc.contributor.authorHofsten, Susannah von
dc.contributor.authorFenton, Kristin Andreassen
dc.contributor.authorPedersen, Hege Lynum
dc.date.accessioned2024-09-26T09:43:07Z
dc.date.available2024-09-26T09:43:07Z
dc.date.issued2024-05-14
dc.description.abstractThe pathogenesis of systemic lupus erythematosus (SLE) is linked to the differential roles of toll-like receptors (TLRs), particularly TLR7, TLR8, and TLR9. TLR7 overexpression or gene duplication, as seen with the Y-linked autoimmune accelerator (Yaa) locus or TLR7 agonist imiquimod, correlates with increased SLE severity, and specific TLR7 polymorphisms and gainof-function variants are associated with enhanced SLE susceptibility and severity. In addition, the X-chromosome location of TLR7 and its escape from X-chromosome inactivation provide a genetic basis for female predominance in SLE. The absence of TLR8 and TLR9 have been shown to exacerbate the detrimental effects of TLR7, leading to upregulated TLR7 activity and increased disease severity in mouse models of SLE. The regulatory functions of TLR8 and TLR9 have been proposed to involve competition for the endosomal trafficking chaperone UNC93B1. However, recent evidence implies more direct, regulatory functions of TLR9 on TLR7 activity. The association between age-associated B cells (ABCs) and autoantibody production positions these cells as potential targets for treatment in SLE, but the lack of specific markers necessitates further research for precise therapeutic intervention. Therapeutically, targeting TLRs is a promising strategy for SLE treatment, with drugs like hydroxychloroquine already in clinical use.en_US
dc.identifier.citationHofsten, Fenton, Pedersen. Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus. International Journal of Molecular Sciences. 2024;25(10)en_US
dc.identifier.cristinIDFRIDAID 2270520
dc.identifier.doi10.3390/ijms25105351
dc.identifier.issn1661-6596
dc.identifier.issn1422-0067
dc.identifier.urihttps://hdl.handle.net/10037/34887
dc.language.isoengen_US
dc.publisherMDPIen_US
dc.relation.journalInternational Journal of Molecular Sciences
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.titleHuman and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosusen_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)
Except where otherwise noted, this item's license is described as Attribution 4.0 International (CC BY 4.0)