Parsing multiomics landscape of activated synovial fibroblasts highlights drug targets linked to genetic risk of rheumatoid arthritis.

导出 LinkOut

翻译打印收藏纠错

作者： Haruka,Tsuchiya ^[1] ; Mineto,Ota ^[1] ; Shuji,Sumitomo ^[2] ; Kazuyoshi,Ishigaki ^[1] ; Akari,Suzuki ^[3] ; Toyonori,Sakata ^[4] ; Yumi,Tsuchida ^[5] ; Hiroshi,Inui ^[1] ; Jun,Hirose ^[6] ; Yuta,Kochi ^[6] ; Yuho,Kadono ^[4] ; Katsuhiko,Shirahige ^[7] ; Sakae,Tanaka ^[8] ; Kazuhiko,Yamamoto ^[5] ; Keishi,Fujio ^[6]

作者单位： Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. ^[1] Department of Functional Genomics and Immunological Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. ^[2] Divisions of Genetics and Rheumatology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. ^[3] Laboratory for Autoimmune Diseases, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan. ^[4] Laboratory of Genome Structure and Function, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, Japan. ^[5] Department of Orthopaedic Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. ^[6] Department of Genomic Function and Diversity, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan. ^[7] Department of Orthopaedic Surgery, Saitama Medical University, Saitama, Japan. ^[8] Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan kfujio-tky@umin.ac.jp. ^[9]

关键词 arthritis autoimmune diseases cytokines fibroblasts rheumatoid synovitis