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. 2010 Jan;49(1):156-66.
doi: 10.1093/rheumatology/kep345. Epub 2009 Nov 23.

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

Tineke Cantaert  1 , Lisa G van Baarsen, Carla A Wijbrandts, Rogier M Thurlings, Marleen G van de Sande, Carina Bos, Tineke C T M van der Pouw Kraan, Cor L Verweij, Paul P Tak, Dominique L Baeten
Affiliations

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

Tineke Cantaert et al. Rheumatology (Oxford). 2010 Jan.

Erratum in

  • Rheumatology (Oxford). 2014 Apr;53(4):770. van der Pouw, Tineke Kraan [corrected to van der Pouw Kraan, Tineke C T M]

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 IFN(high) 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 IFN(low) 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.

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