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Type I interferon signature in Sjögren’s syndrome: pathophysiological and clinical implications


1, 2, 3, 4

 

  1. Department of Physiology, National and Kapodistrian University of Athens, Greece.
  2. Department of Physiology, National and Kapodistrian University of Athens, Greece.
  3. Department of Physiology, National and Kapodistrian University of Athens, Greece.
  4. Departments of Physiology and Pathophysiology, Joint Academic Rheumatology Program, National and Kapodistrian University of Athens, Greece. kmauragan@med.uoa.gr

CER12504
2019 Vol.37, N°3 ,Suppl.118
PI 0185, PF 0191
Reviews

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PMID: 31376268 [PubMed]

Received: 14/06/2019
Accepted : 04/07/2019
In Press: 11/07/2019
Published: 28/08/2019

Abstract

Type I interferons (IFN) have long been recognised as mediators of innate immune defense mechanisms against viral threats. Robust evidence over the last 15 years revealed their significant role in the pathogenesis of systemic autoimmune diseases, including systemic lupus erythematosus (SLE) and Sjögren’s syndrome (SS). Despite the progress, methods of detection, initial triggers, biological functions and clinical associations in the setting of autoimmunity remain to be fully clarified. As therapeutic options for SS are currently limited, neutralising specific targets of the type I IFN pathway seems a promising option. In this review we summarise the current evidence regarding the role of type I IFN in SS.

Rheumatology Article