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10.1002/art.38628

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C4157826!4157826!24644022
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suck abstract from ncbi


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pmid24644022      Arthritis+Rheumatol 2014 ; 66 (6): 1583-95
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  • Modular transcriptional repertoire analyses of adults with systemic lupus erythematosus reveal distinct type I and type II interferon signatures #MMPMID24644022
  • Chiche L; Jourde-Chiche N; Whalen E; Presnell S; Gersuk V; Dang K; Anguiano E; Quinn C; Burtey S; Berland Y; Kaplanski G; Harle JR; Pascual V; Chaussabel D
  • Arthritis Rheumatol 2014[Jun]; 66 (6): 1583-95 PMID24644022show ga
  • Objective: The role for interferon (IFN)-? in systemic lupus erythematosus (SLE) pathogenesis is strongly supported by gene expression studies. The aim of this study was to improve characterization of the blood-IFN signature in adult SLE patients. Methods: Consecutive patients were enrolled and followed-up prospectively. Microarray data were generated using Illumina beadchips. A modular transcriptional repertoire was employed as a framework for the analysis. Results: Our repertoire of 260 modules, which consist of co-clustered gene sets, included 3 IFN-annotated modules (M1.2, M3.4 and M5.12) that were strongly up-regulated in SLE patients. A modular IFN signature (mIS) was observed in 54/62 (87%) patients or 131/157 (83%) longitudinal samples. The IFN signature was more complex than expected with each module displaying a distinct activation threshold (M1.2
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