Transcriptome Analysis of the Interferon-Signature Defining the Autoimmune Process of Sjögren’s Syndrome

Authors

  • A. B. Peck,

    1. Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL, USA
    2. Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL, USA
    3. Center for Orphan Autoimmune Diseases, College of Dentistry, University of Florida, Gainesville, FL, USA
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  • C. Q. Nguyen

    1. Center for Orphan Autoimmune Diseases, College of Dentistry, University of Florida, Gainesville, FL, USA
    2. Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA
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  • The authors state that they have no financial or other conflicts of interest with the content of this study.

A. B. Peck, PhD, Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, PO Box 100275, Gainesville, FL 32610 USA. E-mail: peck@pathology.ufl.edu

Abstract

Sjögren’s syndrome (SS) of humans and SS-like (SjS-like) diseases in mouse models are characterized by chronic immune attacks against the salivary and lacrimal glands leading to exocrine dysfunction. One characteristic of SS and SjS-like diseases repeatedly observed is a strong upregulated expression of both the type I (α/β) and type II (γ) interferons (IFNs). In addition, recent global transcriptome studies have identified a variety of IFN-stimulated gene (ISG) transcripts differentially expressed in tissues of SS patients and mouse models exhibiting SjS-like 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-like diseases being designated as ‘interferon-signature’ diseases. While SS and SjS-like diseases may be designated as such, very little effort has been made to determine what an interferon-signature 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.

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