ACR Meeting Abstracts

ACR Meeting Abstracts

Abstract Number: 1047

Type I and II Interferon Signatures in Sjogren’s Syndrome: Contributions in Distinct Clinical Phenotypes and Sjogren’s Related Lymphomagenesis

Adrianos Nezos1, Fotini Gravani2, Efstathia K. Kapsogeorgou3, Michael Voulgarelis4, Haralampos M. Moutsopoulos4, Mary K. Crow5 and Clio Mavragani6, 1Department of Physiology, School of Medicine, University of Athens, Athens, Greece, 2Department of Rheumatology, General Hospital of Athens "G.Gennimatas", Athens, Greece, 3Pathophysiology, School of Medicine, National University of Athens, Greece, Athens, Greece, 4Department of Pathophysiology, School of Medicine, University of Athens, Athens, Greece, 5Department of Medicine, Hospital for Special Surgery, New York, NY, 6Department of Physiology, School of Medicine, University of Athens, Athens, Greece

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords:

Session Information

Title: Cytokines, Mediators, Cell-cell Adhesion, Cell Trafficking and Angiogenesis

Session Type: Abstract Submissions (ACR)

Background/Purpose: Both type I and II interferons (IFNs) have been implicated in the pathogenesis of Sjogren’s syndrome (SS). We aimed to explore the contribution of type I and II IFN signatures in the generation of distinct SS clinical phenotypes including non-Hodgkin’s lymphoma (NHL) development, a major SS complication.  

Methods: Peripheral blood from SS patients (n=31), SS patients complicated by lymphoma (SSL, n=13) and healthy donors (HD, n=30) were subjected to real-time polymerase chain reaction for 3 interferon inducible genes (IFIGs) preferentially induced by type I IFN, 2 IFIGs preferentially induced by IFNγ as well as for IFNα and IFNγ genes.  The same analysis was performed in minor salivary gland tissues (MSG) derived from 31 SS patients, 10 SSL patients and 17 sicca controls (SC). 

Results: In peripheral blood and MSG tissues, overexpression of both type I and type II IFIGs was observed in SS patients versus HC and SC, respectively, with a predominance of type I IFN signature in peripheral blood and a type II IFN signature in MSG tissues. SS patients with salivary gland enlargement, lymphopenia, anti-Ro/SSA antibodies and hypergammaglobulinemia exhibited higher type I IFN scores in peripheral blood compared to their counterparts without those features. Hypergammaglobulinemia was also associated with increased type II IFN scores in peripheral blood. In MSG tissues derived from SSL patients we observed lower IFNα, but higher IFNγ and type II IFIG transcripts compared to both SS and SC. In ROC curve analysis, IFNγ/IFNα ratio in MSG tissues showed the best discrimination for lymphoma development, with an area under the curve of 0.88 (95% CI:0.72-1.00, p-value: 0.001).  

Conclusion: Discrete expression patterns of type I and II IFN signatures might be related to distinct clinical SS features and SS related lymphomagenesis

Disclosure:

A. Nezos,
None;

F. Gravani,
None;

E. K. Kapsogeorgou,
None;

M. Voulgarelis,
None;

H. M. Moutsopoulos,
None;

M. K. Crow,
None;

C. Mavragani,
None.

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