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dc.contributor.authorEilertsen, Gro Østli
dc.contributor.authorGhelue, Marijke van
dc.contributor.authorNossent, Johannes C
dc.date.accessioned2013-01-10T11:58:09Z
dc.date.available2013-01-10T11:58:09Z
dc.date.issued2012
dc.description.abstractB cell activating factor (BAFF) inhibitor therapy has recently been approved for non-renal Systemic Lupus Erythematosus (SLE). While BAFF plays a role in experimental lupus nephritis (LN), its role human LN is not well studied. Case control study in 102 SLE patients, 30 with LN (+LN) and 72 without LN (-LN) and 31 healthy controls. We analysed BAFF mRNA expression in PBMCs (BAFF-RQ) and serum BAFF (s-BAFF) levels and investigated their relation with clinical, histological- and additional acute phase proteins. Results: s-BAFF and BAFF-RQ were increased in +LN patients compared to controls, but their expression did not correlate with ISN/RPS class, Activity- or Chronicity index on biopsy. s-BAFF correlated with levels of anti-nucleosome antibodies, C1 inhibitor and α-1-acid-glycoprotein (AGP), while BAFF-RQ correlated inversely with Factor VIII. s-BAFF and BAFF mRNA levels are increased in LN patients, but do not reflect histological disease severity. The association of increased BAFF expression with both pro- and anti-inflammatory markers and reduced endothelial activation suggest that BAFF inhibition in LN may have diverse effects.en
dc.identifier.citationJournal of Data Mining in Genom Protemics (2012), vol 3, no. 1en
dc.identifier.cristinIDFRIDAID 866004
dc.identifier.doidoi: 10.4172/2153-0602.1000113
dc.identifier.issn1536-2310
dc.identifier.urihttps://hdl.handle.net/10037/4748
dc.identifier.urnURN:NBN:no-uit_munin_4459
dc.language.isoengen
dc.publisherData Mining in Genomics & Protemicsen
dc.rights.accessRightsopenAccess
dc.subjectVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Rheumatology: 759en
dc.subjectVDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Reumatologi: 759en
dc.titleBAFF expression is increased in Lupus Nephritis and associated with activation of C1 inhibitor, α-1-acid-glycoprotein and endothelial markers.en
dc.typeJournal articleen
dc.typeTidsskriftartikkelen
dc.typePeer revieweden


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