p53 in fibroblast-like synoviocytes can regulate T helper cell functions in patients with active rheumatoid arthritis

作     者：TANG Bi-xia YOU Xin ZHAO Li-dan LI Yang ZHANG Xuan TANG Fu-lin BA De-nian HE Wei 

作者机构：Department of Rheumatology Peking Union Medical College Hospital Chinese Academy of Medical Sciences & Peking Union Medical College Beijing 100032 China Department of Immunology School of Basic Medicine Peking Union Medical College and Institute of Basic Medical SciencesChinese Academy of Medical Sciences Beijing 100005 China 

出 版 物：《Chinese Medical Journal》 (中华医学杂志（英文版）)

年 卷 期：2011年第124卷第3期

页      面：364-368页

核心收录：

学科分类：0710[理学-生物学] 1007[医学-药学(可授医学、理学学位)] 100704[医学-药物分析学] 07[理学] 071009[理学-细胞生物学] 09[农学] 0901[农学-作物学] 090102[农学-作物遗传育种] 10[医学] 

基　　金：国家教育部新世纪优秀人才支持计划 国家自然科学基金 National Program for Key Basic Research Project, Ministry of Science and Technology, China for Immunology 

主　　题：rheumatoid arthritis p53 helper T-cells 

摘      要：Background p53 is a tumor suppressor and plays a key role in regulating cell hyperplasia, repairing DNA and inducing apoptosis. This study was to investigate p53 expression in fibroblast-like synoviocytes （FLS） and its effect on CD4＋ T lymphocytes from patients with active rheumatoid arthritis （RA）.Methods Human FLS were transfected with p53 siRNA and cocultured with CD4＋ T lymphocytes from patients with active RA. The expressions of osteoprotegerin and interleukin （IL）-6 were detected in p53 siRNA and scramble siRNA-transfected FLS. In addition, protein levels of interferon （IFN）-γ, IL-17, IL-4 and CD25 as well as mRNAs of IFN-γ,retinoic acid-related orphan receptor （ROR）-γt, IL-17 and Foxp3 in cocultured CD4＋ T lyrmphocytes were also *** IL-6 decreased in p53-knockdown FLS while osteoprotegerin expression was not altered. FLS with p53 deletion significantly increased the production of IL-17 and IFN-γ by CD4＋ T cells and upregulated Foxp3 mRNA expression without effects on the proportion of CD4＋CD25high T *** p53 in FLS might regulate Th1 and Th17 functions in patients with RA and participate in the pathogenesis of RA.