Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/67627
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dc.contributor.authorSatoh, M.
dc.contributor.authorChan, J.Y.F.
dc.contributor.authorCeribelli, A.
dc.contributor.authorDel-Mercado, M.V.
dc.contributor.authorChan, E.K.L.
dc.date.accessioned2015-11-19T18:52:20Z-
dc.date.available2015-11-19T18:52:20Z-
dc.date.issued2013
dc.identifier.urihttp://hdl.handle.net/20.500.12104/67627-
dc.description.abstractLike many other classical autoantibodies in systemic rheumatic diseases, anti-Su antibodies were originally defined by the double immunodiffusion assay in the early 80s. However, despite its high prevalence, only a few reports on anti-Su were published in the following years and the progress in characterizing the target antigens and clinical significance was slow, probably due to its inconsistent or poor reactivity in other standard immunoassays. In 2006 the target antigen was identified as the microRNA (miRNA)-binding protein Argonaute 2 (Ago2). Ago2 is a key component of the RNA-induced silencing complex enriched in cytoplasmic foci called GW bodies. Due to preferential reactivity of human autoantibodies with native antigens, immunoprecipitation is the only method to reliably detect anti-Su/Ago2 antibodies. Anti-Su/Ago2 does not appear to have disease specificity since it is found in 10-20% of patients with various rheumatic diseases, including systemic lupus erythematosus, scleroderma, polymyositis/dermatomyositis, and Sjögren's syndrome, as well as apparently healthy individuals at lower prevalence. The clinical significance and the mechanism of production of anti-Su/Ago2 remains to be clarified. © Springer Science+Business Media New York 2013.
dc.titleAutoantibodies to argonaute 2 (su antigen)
dc.typeArticle
dc.identifier.doi10.1007/978-1-4614-5107-5-4
dc.relation.ispartofjournalAdvances in Experimental Medicine and Biology
dc.relation.ispartofvolume768
dc.relation.ispartofpage45
dc.relation.ispartofpage59
dc.contributor.affiliationSatoh, M., Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Florida, P.O. Box 100221, Gainesville, FL 32610-0221, United States; Chan, J.Y.F., Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Florida, P.O. Box 100221, Gainesville, FL 32610-0221, United States; Ceribelli, A., Clinical Immunology, Humanitas Clinical and Research Center, Rozzano, Italy; Del-Mercado, M.V., Instituto de Investigacion en Reumatologia y del Sistema Musculo Esqueletico, Centro Universitario de Ciencias de la Salud, Hospital Civil de Guadalajara Dr. Juan I. Menchaca, Salvador de Quevedo y Zubieta # 750 S.L, Guadalajara, Jalisco, Mexico; Chan, E.K.L., Department of Oral Biology, University of Florida, PO Box 100424, Gainesville, FL 32610, United States
dc.relation.isReferencedByScopus
dc.relation.isReferencedByWOS
dc.identifier.urlhttp://www.scopus.com/inward/record.url?eid=2-s2.0-84873557531&partnerID=40&md5=ceecec9c490c00d8346db20238755651
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