PMID- 29387065
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231112
IS  - 1664-3224 (Print)
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 8
DP  - 2017
TI  - Heterogeneity of the Type I Interferon Signature in Rheumatoid Arthritis: A 
      Potential Limitation for Its Use As a Clinical Biomarker.
PG  - 2007
LID - 10.3389/fimmu.2017.02007 [doi]
LID - 2007
AB  - INTRODUCTION: An increased expression of interferon (IFN)-responding genes 
      (IRGs), the so-called IFN signature, has been reported in rheumatoid arthritis 
      (RA). However, some controversy exists concerning its clinical relevance. The 
      main aim of this study is to evaluate whether quantitative and qualitative 
      differences in the activation of the IFN pathway may account for these findings. 
      METHODS: The expression of IFN-induced protein 44 (IFI44), IFN-induced protein 44 
      like (IFI44L), IFN alpha inducible protein 6, and MX dynamin-like GTPase 1 (MX1) 
      was determined in peripheral blood in 98 RA patients (IFI6) and 28 controls. RA 
      patients were classified into groups according to their clinical stage and 
      treatments received: very early RA (VERA), biological disease-modifying 
      antirheumatic drug (bDMARD) naive, and bDMARD. An additional group of 13 RA 
      patients candidates for tumor necrosis factor alpha (TNFalpha) blockade was also 
      recruited. The associations among IRGs were evaluated by network and principal 
      component analyses. RESULTS: The expression of all IRGs was increased in RA to 
      different levels. The IFN score was increased in all RA groups (VERA, 
      bDMARD-naive, and bDMARD), but important differences in their degree of 
      activation and in the relationships among IRGs were observed. The IFN score 
      correlated with the accumulated disease activity score 28-joints, and it was 
      found to be a predictor of clinical outcome in VERA. No differences in the IFN 
      score were observed between the bDMARD-naive and bDMARD groups, but opposite 
      associations with the clinical parameters were noted. Interestingly, the 
      correlations among IRGs delineate different pictures between these two groups. 
      The IFN score at baseline predicted poor clinical outcome upon TNFalpha blockade. 
      Although no absolute changes in the IFN score were found, TNFalpha-blockade shifted 
      the associations among IRGs. CONCLUSION: A certain heterogeneity within the IFN 
      signature can be recognized in RA, depending on the clinical stage. The structure 
      of the IFN signature may be a potential explanation for the controversy in this 
      field and must be considered to decipher its clinical relevancein RA.
FAU - Rodriguez-Carrio, Javier
AU  - Rodriguez-Carrio J
AD  - Area of Immunology, Department of Functional Biology, Faculty of Medicine, 
      University of Oviedo, Oviedo, Spain.
AD  - Instituto de Investigacion Sanitaria del Principado de Asturias (ISPA), Oviedo, 
      Spain.
FAU - Alperi-Lopez, Mercedes
AU  - Alperi-Lopez M
AD  - Instituto de Investigacion Sanitaria del Principado de Asturias (ISPA), Oviedo, 
      Spain.
AD  - Department of Rheumatology, Hospital Universitario Central de Asturias, Oviedo, 
      Spain.
FAU - Lopez, Patricia
AU  - Lopez P
AD  - Area of Immunology, Department of Functional Biology, Faculty of Medicine, 
      University of Oviedo, Oviedo, Spain.
AD  - Instituto de Investigacion Sanitaria del Principado de Asturias (ISPA), Oviedo, 
      Spain.
FAU - Ballina-Garcia, Francisco J
AU  - Ballina-Garcia FJ
AD  - Instituto de Investigacion Sanitaria del Principado de Asturias (ISPA), Oviedo, 
      Spain.
AD  - Department of Rheumatology, Hospital Universitario Central de Asturias, Oviedo, 
      Spain.
FAU - Suarez, Ana
AU  - Suarez A
AD  - Area of Immunology, Department of Functional Biology, Faculty of Medicine, 
      University of Oviedo, Oviedo, Spain.
AD  - Instituto de Investigacion Sanitaria del Principado de Asturias (ISPA), Oviedo, 
      Spain.
LA  - eng
PT  - Journal Article
DEP - 20180116
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
PMC - PMC5775969
OTO - NOTNLM
OT  - IFN signature
OT  - arthritis
OT  - autoimmunity
OT  - biomarker
OT  - interferon
EDAT- 2018/02/02 06:00
MHDA- 2018/02/02 06:01
PMCR- 2017/01/01
CRDT- 2018/02/02 06:00
PHST- 2017/11/23 00:00 [received]
PHST- 2017/12/27 00:00 [accepted]
PHST- 2018/02/02 06:00 [entrez]
PHST- 2018/02/02 06:00 [pubmed]
PHST- 2018/02/02 06:01 [medline]
PHST- 2017/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2017.02007 [doi]
PST - epublish
SO  - Front Immunol. 2018 Jan 16;8:2007. doi: 10.3389/fimmu.2017.02007. eCollection 
      2017.