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Association of endogenous anti–interferon‐α autoantibodies with decreased interferon‐pathway and disease activity in patients with systemic lupus erythematosus

dc.contributor.authorMorimoto, Alyssa M.en_US
dc.contributor.authorFlesher, Donna Thibaulten_US
dc.contributor.authorYang, Jihongen_US
dc.contributor.authorWolslegel, Kristenen_US
dc.contributor.authorWang, Xiangdanen_US
dc.contributor.authorBrady, Annen_US
dc.contributor.authorAbbas, Alexander R.en_US
dc.contributor.authorQuarmby, Valerieen_US
dc.contributor.authorWakshull, Ericen_US
dc.contributor.authorRichardson, Bruce C.en_US
dc.contributor.authorTownsend, Michael J.en_US
dc.contributor.authorBehrens, Timothy W.en_US
dc.date.accessioned2011-11-10T15:38:30Z
dc.date.available2012-10-01T18:34:42Zen_US
dc.date.issued2011-08en_US
dc.identifier.citationMorimoto, Alyssa M.; Flesher, Donna Thibault; Yang, Jihong; Wolslegel, Kristen; Wang, Xiangdan; Brady, Ann; Abbas, Alexander R.; Quarmby, Valerie; Wakshull, Eric; Richardson, Bruce; Townsend, Michael J.; Behrens, Timothy W. (2011). "Association of endogenous anti–interferon‐α autoantibodies with decreased interferon‐pathway and disease activity in patients with systemic lupus erythematosus." Arthritis & Rheumatism 63(8): 2407-2415. <http://hdl.handle.net/2027.42/87110>en_US
dc.identifier.issn0004-3591en_US
dc.identifier.issn1529-0131en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/87110
dc.description.abstractObjective Numerous observations implicate interferon‐α (IFNα) in the pathophysiology of systemic lupus erythematosus (SLE); however, the potential impact of endogenous anti‐IFNα autoantibodies (AIAAs) on IFN‐pathway and disease activity is unclear. The aim of this study was to characterize IFN‐pathway activity and the serologic and clinical profiles of AIAA‐positive patients with SLE. Methods Sera obtained from patients with SLE (n = 49), patients with rheumatoid arthritis (n = 25), and healthy control subjects (n = 25) were examined for the presence of AIAAs, using a biosensor immunoassay. Serum type I IFN bioactivity and the ability of AIAA‐positive sera to neutralize IFNα activity were determined using U937 cells. Levels of IFN‐regulated gene expression in peripheral blood were determined by microarray, and serum levels of BAFF, IFN‐inducible chemokines, and other autoantibodies were measured using immunoassays. Results AIAAs were detected in 27% of the serum samples from patients with SLE, using a biosensor immunoassay. Unsupervised hierarchical clustering analysis identified 2 subgroups of patients, IFN low and IFN high , that differed in the levels of serum type I IFN bioactivity, IFN‐regulated gene expression, BAFF, anti–ribosomal P, and anti‐chromatin autoantibodies, and in AIAA status. The majority of AIAA‐positive patients had significantly lower levels of serum type I IFN bioactivity, reduced downstream IFN‐pathway activity, and lower disease activity compared with the IFN high patients. AIAA‐positive sera were able to effectively neutralize type I IFN activity in vitro. Conclusion Patients with SLE commonly harbor AIAAs. AIAA‐positive patients have lower levels of serum type I IFN bioactivity and evidence for reduced downstream IFN‐pathway and disease activity. AIAAs may influence the clinical course in SLE by blunting the effects produced by IFNα.en_US
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.titleAssociation of endogenous anti–interferon‐α autoantibodies with decreased interferon‐pathway and disease activity in patients with systemic lupus erythematosusen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelGeriatricsen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumAnn Arbor VA Hospital, Ann Arbor, Michigan and University of Michigan, Ann Arboren_US
dc.contributor.affiliationotherGenentech, South San Francisco, Californiaen_US
dc.contributor.affiliationotherAmgen, South San Francisco, Californiaen_US
dc.contributor.affiliationotherDepartment of Bioanalytical Research and Development MS‐38, Genentech, 1 DNA Way, South San Francisco, CA 94080en_US
dc.identifier.pmid21506093en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/87110/1/30399_ftp.pdf
dc.identifier.doi10.1002/art.30399en_US
dc.identifier.sourceArthritis & Rheumatismen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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