EBV and other viruses as triggers of tertiary lymphoid structures in primary Sjögren's syndrome. (April 2014)

• Record Type: Journal Article
• Authors: Lucchesi, Davide; Pitzalis, Costantino; Bombardieri, Michele
• Is Part Of: Expert review of clinical immunology. Volume 10:Number 4(2014)
• Page Start: 445
• Page End: 455
• Publication Date: 2014-04
• Subjects: Clinical immunology -- Periodicals; 616.079
• DOI: 10.1586/1744666X.2014.892417
• Languages: English
• ISSNs: 1744-666X

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <p>Sjögren's syndrome (SS) is an autoimmune disease that targets salivary (SG) and lachrymal glands, leading to exocrine dysfunction. Several viruses have been associated with SS, although the role of persistent viral infections in triggering and/or perpetuating the disease is still a matter of controversy. Together with exocrine dysfunction, SS is characterised by the production of autoantibodies and the presence of lymphomonocytic periductal aggregates in the SG, which in 30/40% of the patients display features of tertiary lymphoid structures (TLS) supporting an ectopic germinal centre response. Here we first review i) the relevance of TLS in SS and ii) the evidence in support of a role for viruses in SS insurgence and/or persistence; next, iii) we review recent data which links viral infection with TLS formation in the SG and suggests that viral-host interactions within TLS favour breach of tolerance and development of autoimmunity in SS.</p> </abstract>