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One characteristic of SS and SjS\u2010like diseases repeatedly observed is a strong upregulated expression of both the type I (\u03b1\/\u03b2) and type II (\u03b3) interferons (IFNs). In addition, recent global transcriptome studies have identified a variety of IFN\u2010stimulated gene (ISG) transcripts differentially expressed in tissues of SS patients and mouse models exhibiting SjS\u2010like disease. Analyses of these transcriptome databases indicate that the sets of differentially expressed genes are highly restricted, suggesting that there is a unique specificity in ISGs activated (or suppressed) during development and onset of disease. As a result, these observations have led to both SS and SjS\u2010like diseases being designated as \u2018interferon\u2010signature\u2019 diseases. While SS and SjS\u2010like diseases may be designated as such, very little effort has been made to determine what an interferon\u2010signature might signify relative to autoinflammation and whether it might point directly to an underlying etiopathological mechanism. Here, we review these limited data and provide a model of how the products of these genes interact molecularly and biologically to define critical details of SS pathology.<\/jats:p>","DOI":"10.1111\/j.1365-3083.2012.02749.x","type":"journal-article","created":{"date-parts":[[2012,6,16]],"date-time":"2012-06-16T03:38:36Z","timestamp":1339817916000},"page":"237-245","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Transcriptome Analysis of the Interferon\u2010Signature Defining the Autoimmune Process of Sj\u00f6gren\u2019s Syndrome"],"prefix":"10.1111","volume":"76","author":[{"given":"A. 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