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Abstract Number: 1656

Interferon Type I and T Helper 17: A Dangerous Liaison In Primary Sjögren’s Syndrome?

Zana Brkic1, Sandra M.J. Paulissen2, Cornelia G. van Helden-Meeuwsen3, Naomi I. Maria3, Odilia B.J. Corneth4, Nadine Davelaar5, Jan Piet van Hamburg5, Paul L. Van Daele3, Virgil A. Dalm1, Martin van Hagen3, Erik Lubberts6 and Marjan A. Versnel1, 1Erasmus Medical Center, Immunology, Rotterdam, Netherlands, 2Rheumatology, Erasmus Medical Center, Rotterdam, Netherlands, 3Immunology, Erasmus Medical Center, Rotterdam, Netherlands, 4Rheumatology and Immunology, Erasmus Medical Center, Rotterdam, Netherlands, 5Immunology, Erasmus MC, University Medical Center, Rotterdam, Netherlands, 6Erasmus Medical Center, Rheumatology, Rotterdam, Netherlands

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Autoimmunity, cytokines and interferons, Sjogren's syndrome, T cells

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Session Information

Session Title: T-cell Biology in Autoimmune Diseases

Session Type: Abstract Submissions (ACR)

Background/Purpose:

The T helper 17 (Th17) cell subset, which produces IL-17A, IL-17F, IL-22 and IL-21, has been implicated in the pathogenesis of primary Sjögren’s syndrome (pSS). The aim of this study was to elucidate a possible link between the Th17 system and another key-player in the pathogenesis of pSS ¯ Interferon (IFN) type I.

Methods:

IFN type I signature was assessed by mRNA expression of IFN type I inducible genes. Th cell populations were analyzed by flow cytometry in peripheral blood of 12 pSS patients positive (IFN+) and 12 patients negative (IFN-) for the IFN type I signature and 12 healthy controls (HC). Cytokine expression by memory Th cells (CD4+CD45RO+) cells and memory CCR6+ Th cells (CD4+CD45RO+CCR6+) cells was assessed.

Results:

Th17 (defined as CD4+CD45RO+CCR6+CCR4+CXCR3-CCR10-) and Treg cell percentages were significantly increased in IFN+ patients compared with IFN- patients and HC. This was accompanied by a significant decrease in Th1 cells in IFN+ patients compared to HC. IL-22 and IL-21 production by memory Th cells and memory CCR6+ cells was higher in IFN+ patients. Interestingly, Th17 cell percentage was significantly correlated with presence of anti-SSA antibodies, hypergammagloblulinemia and elevated expression of monocyte B cell activating factor (BAFF) , all three previously found in IFN type I signature positive patients.

Conclusion:

Here we show for the first time a relation between two key players of pSS pathogenesis − IFN type I and the Th17 pathway. This study brings new insights in the pathogenesis of pSS, having possible implications for future treatment.


Disclosure:

Z. Brkic,
None;

S. M. J. Paulissen,
None;

C. G. van Helden-Meeuwsen,
None;

N. I. Maria,
None;

O. B. J. Corneth,
None;

N. Davelaar,
None;

J. P. van Hamburg,
None;

P. L. Van Daele,
None;

V. A. Dalm,
None;

M. van Hagen,
None;

E. Lubberts,
None;

M. A. Versnel,
None.

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