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Rheumatology Advance Access published online on November 23, 2009
Rheumatology, doi:10.1093/rheumatology/kep345
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© The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Type I interferons have no major influence on humoral autoimmunity in rheumatoid arthritis

Tineke Cantaert1,*, Lisa G. van Baarsen1,2,*, Carla A. Wijbrandts1, Rogier M. Thurlings1, Marleen G. van de Sande1, Carina Bos2, Tineke Kraan van der Pouw3, Cor L. Verweij2, Paul P. Tak1 and Dominique L. Baeten1

1Department of Clinical Immunology and Rheumatology, Academic Medical Center/University of Amsterdam, 2Department of Pathology, VU Medical Center and 3Department of Molecular Cell Biology and Immunology, VU Medical Center, Amsterdam, The Netherlands.

Correspondence to: Dominique Baeten, Department of Clinical Immunology and Rheumatology, F4-218, Academic Medical Center/University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. E-mail: d.l.baeten{at}amc.uva.nl.


  Abstract

Objective. Type I IFNs have recently been implicated in autoantibody-mediated diseases such as SLE. As half the RA patients display a type I IFNhigh signature, we investigated in a pilot study if type I IFN determines the autoantibody response in RA.

Methods. Serum and peripheral blood cells were obtained from 52 RA patients, with paired samples before and after infliximab treatment in 21 patients. Additional samples were collected from 8 anti-citrullinated protein antibody (ACPA)-positive individuals without arthritis and from 10 ACPA-negative healthy controls. The type I IFN signature was determined by peripheral blood cell gene expression analysis and quantitative RT–PCR. ACPA IgG and IgM, RF IgM, anti-nucleosome IgM and anti-dsDNA were measured by ELISA.

Results. The type I IFN signature was not related to the presence and titers of ACPA and RF during active disease. TNF blockade induced a similar rise of ANAs, and a similar decrease in RF titers in both groups. ACPA IgG and IgM levels appeared to be down-modulated only in the type I IFNlow group. These changes were independent of the changes in type I IFN response gene activity after TNF blockade. Furthermore, the ACPA response in individuals without arthritis and inflammation was not related to an increase of type I IFN.

Conclusions. In this explorative study, type I IFN signature does not appear to have a major impact on the humoral autoimmune response in RA. Replication of these data remains warranted.

KEY WORDS: Type I interferon, Rheumatoid arthritis, Autoantibodies, Anti-citrullinated protein antibody

*Tineke Cantaert and Lisa G. van Baarsen equally contributed to this work.

Submitted 21 May 2009; revised version accepted 25 September 2009.
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