title: Type I interferon response gene expression in established rheumatoid arthritis is not associated with clinical parameters.
abstract: A peripheral blood interferon (IFN) signature (i.e., elevated type I interferon response gene [IRG] expression) has been described in a subset of patients with rheumatoid arthritis (RA). In the present study, we systematically assessed the association between this IRG expression and clinical parameters.
  
  
  
  Expression of 19 IRGs was determined in peripheral blood from 182 consecutive patients with RA and averaged into an IFN score per individual. Correlation and unpaired analyses were performed on the complete patient group. The analyses were internally validated by using an algorithm to randomize the patient group 1000 times into two equally sized sets, and then analyses were performed on both sets.
  
  
  
  Associations were assessed between IFN score and disease duration, 28-joint Disease Activity Score and its components, the occurrence of erosions and nodules, autoantibody positivity, and immunosuppressive treatment. This analysis revealed lower IFN scores in patients using hydroxychloroquine, prednisone, and/or sulfasalazine, but it did not show significant associations between the other parameters and the IFN score. Selecting patients who were not treated with hydroxychloroquine, prednisone, and/or sulfasalazine (n = 95) did not reveal any significant associations either.
  
  
  
  IRG expression in RA is affected by immunosuppressive treatment with prednisone, hydroxychloroquine, and/or sulfasalazine, but it is not evidently associated with other clinical parameters. Hence, the IFN signature appears to describe a subgroup of patients with RA but does not seem to reflect disease activity.
authors.affiliation: Amsterdam Rheumatology and Immunology Center, VU University Medical Center, CCA 2.21, P.O. Box 7075, 1007MB, Amsterdam, The Netherlands. td.dejong@vumc.nl.
authors.forename: Tamarah D
authors.initials: TD
authors.lastname: de Jong
authors.affiliation: Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands.
authors.forename: Marjolein
authors.initials: M
authors.lastname: Blits
authors.affiliation: Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands.
authors.forename: Sander
authors.initials: S
authors.lastname: de Ridder
authors.affiliation: Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands.
authors.forename: Saskia
authors.initials: S
authors.lastname: Vosslamber
authors.affiliation: Amsterdam Rheumatology and Immunology Center, Reade, Amsterdam, The Netherlands.
authors.forename: Gertjan
authors.initials: G
authors.lastname: Wolbink
authors.affiliation: Amsterdam Rheumatology and Immunology Center, Reade, Amsterdam, The Netherlands.
authors.forename: Mike T
authors.initials: MT
authors.lastname: Nurmohamed
authors.affiliation: Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands.
authors.forename: Cornelis L
authors.initials: CL
authors.lastname: Verweij
mesh_terms: D000328:Adult; D000368:Aged; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000188:drug therapy / Q000473:pathology*; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007370:Interferon Type I / Q000096:biosynthesis* / Q000097:blood; D008297:Male; D008875:Middle Aged; D060888:Real-Time Polymerase Chain Reaction; D059467:Transcriptome
chemical_list: D018501:Antirheumatic Agents; D007166:Immunosuppressive Agents; D007370:Interferon Type I
keywords: Gene expression; Rheumatoid arthritis; Type I interferon