targeting histone deacetylase activity in rheumatoid arthritis and asthma as prototypes of inflammatory disease should we keep our hats on针对类风湿性关节炎和哮喘组蛋白脱乙酰酶活动的原型炎性疾病我们应该保持我们的帽子.pdfVIP

Available online /content/10/5/226 Review Targeting histone deacetylase activity in rheumatoid arthritis and asthma as prototypes of inflammatory disease: should we keep our HATs on? Aleksander M Grabiec, Paul P Tak and Kris A Reedquist Division of Clinical Immunology and Rheumatology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands Corresponding author: Kris A Reedquist, k.a.reedquist@amc.uva.nl Published: 17 October 2008 Arthritis Research Therapy 2008, 10:226 (doi:10.1186/ar2489) This article is online at /content/10/5/226 © 2008 BioMed Central Ltd Abstract distinct components of this network, such as TNFα, IL-1, IL-6 Cellular activation, proliferation and survival in chronic inflammatory and receptor activator of NFκB ligand, contribute to diseases is regulated not only by engagement of signal trans- inflammation and joint destruction in RA have been translated duction pathways that modulate transcription factors required for into innovative and increasingly successful treatment of these processes, but also by epigenetic regulation of transcription patients in the clinic [1]. Many of the extracellular stimuli factor access to gene promoter regions. Histone acetyl trans- driving pathology in RA do so through the activation of con- ferases coordinate the recruitment and activation of transcription served intracellular signaling proteins and pathways, inclu- factors with conformational changes