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Abstract Number: 528

Mxa As a Biomarker for Systemic Interferon Type I Activation in Primary Sjögren′s Syndrome

Naomi I. Maria1, Zana Brkic1, Matti Waris2, Cornelia G. van Helden-Meeuwsen1, Kim Heezen1, Joop P. van de Merwe1, Paul L. van Daele3, Virgil A. Dalm3, Hemmo A. Drexhage3 and Marjan A. Versnel3, 1Immunology, Erasmus Medical Center, Rotterdam, Netherlands, 2Department of Virology, University of Turku, Turku, Finland, 3Erasmus Medical Center, Immunology, Rotterdam, Netherlands

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: interferons and monocytes, Sjogren's syndrome

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Session Information

Title: Sjögren's Syndrome - Pathogenesis

Session Type: Abstract Submissions (ACR)

Background/Purpose: To establish an easy and practical assay for detection of systemic Interferon (IFN) type I activation in primary Sjögren’s syndrome (pSS). The monocyte IFN type I signature is present in over half of pSS patients and identifies a subgroup of patients with higher clinical disease activity [Z. Brkic et al., 2012]. Currently, detection of the IFN type I signature is performed via laborious mRNA expression profiles of multiple IFN type I inducible genes. Methods: In a cohort of 35 pSS patients Myxovirus resistance protein A (MxA) was tested as potential biomarker for systemic IFN type bioactivity. An MxA-enzyme immunoassay (EIA) on whole blood was compared with flow cytometric detection of MxA in CD14+ monocytes. In addition CD64 (Fcγ RI), CD169 (Siglec-1) and BAFF (B-cell activating factor), previously described as biomarkers for IFN type I in other systemic autoimmune diseases, were assessed in CD14+ monocytes using flow cytometry. The IFNscore, a measure for total IFN type I activation, was calculated using expression values of the IFN type I signature genes – IFI44, IFI44L, IFIT3, LY6E, MX1 – in CD14+ monocytes, determined by real-time quantitative PCR. pSS patients were stratified in an IFN-positive (IFNscore>10) and IFN-negative pSS subgroup (IFNscore<10). Results: Twenty-one out of 35 pSS patients were IFN-positive (IFNpos), whereas HC were negative for the IFN type I signature. Significant correlations were found between IFNscores and CD14+ monocyte protein expression of MxA (p<0.001;r=0.733), CD64 (p=0.007;r=0.436), CD169 (p<0.001;r=0.495) and MxA protein expression in whole blood (p<0.001;r=0.717). MxA assessed by the MxA-EIA showed significantly elevated levels in IFNpos patients with a median of 212.5 (10-1295) µg/l, whereas IFNneg patients [1µg/l(1-330)] expressed MxA at levels equal to HC [15µg/l(1-150)] (p<0.001). Similar results were obtained for MxA assessed by flow cytometry (p<0.001). MxA-EIA protein levels correlated with the EULAR Sjögren’s syndrome Disease Activity Index score; Immunoglobulin levels; rheumatoid factor; haemoglobin levels and neutrophil counts. Conclusion: MxA protein analysis is a promising tool for assessment of IFN type I activation in pSS. MxA levels determined by MxA-EIA correlated with features of disease activity. The EIA was shown to be a functional assay and could contribute to future studies on disease pathogenesis and pSS subclassification, possibly leading to more targeted treatment strategies.

 

 


Disclosure:

N. I. Maria,

Not apllicable,

3;

Z. Brkic,
None;

M. Waris,
None;

C. G. van Helden-Meeuwsen,
None;

K. Heezen,
None;

J. P. V. D. Merwe,
None;

P. L. V. Daele,
None;

V. A. Dalm,
None;

H. A. Drexhage,
None;

M. A. Versnel,

Not applicable,

2.

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