MINI REVIEW ARTICLE
Front. Immunol., 20 September 2013 | doi: 10.3389/fimmu.2013.00290
- 1Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA
- 2Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
Sjögren’s syndrome (SS) is a common, progressive autoimmune exocrinopathy distinguished by dry eyes and mouth and affects ∼0.7% of the European population. Overexpression of transcripts induced by interferons (IFN), termed as an “IFN signature,” has been found in SS patients. Four microarray studies have been published in SS that identified dysregulated genes within type I IFN signaling in either salivary glands or peripheral blood of SS patients. The mechanism of this type I IFN activation is still obscure, but several possible explanations have been proposed, including virus infection-initiated and immune complex-initiated type I IFN production by plasmacytoid dendritic cells. Genetic predisposition to increased type I IFN signaling is supported by candidate gene studies showing evidence for association of variants within IFN-related genes. Once activated, IFN signaling may contribute to numerous aspects of SS pathophysiology, including lymphocyte infiltration into exocrine glands, autoantibody production, and glandular cell apoptosis. Thus, dysregulation of IFN pathways is an important feature that can be potentially used as a serum biomarker for diagnosis and targeting of new treatments in this complex autoimmune disease.
Keywords: interferon signature, Sjögren’s syndrome, gene expression profiling, microarrays, type I interferon, genetic association, mechanisms, biomarker
Citation: Li H, Ice JA, Lessard CJ and Sivils KL (2013) Interferons in Sjögren’s syndrome: genes, mechanisms, and effects. Front. Immunol. 4:290. doi: 10.3389/fimmu.2013.00290
Received: 08 July 2013; Paper pending published: 26 July 2013;
Accepted: 04 September 2013; Published online: 20 September 2013.
Accepted: 04 September 2013; Published online: 20 September 2013.
Edited by:
Timothy B. Niewold, Mayo Clinic, USA
Copyright: © 2013 Li, Ice, Lessard and Sivils. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Kathy L. Sivils, Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, 825 N.E. 13th Street, MS57, Oklahoma City, OK 73104, USA e-mail: sivilsk@omrf.org
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