ナカヤマ リョウコ   Nakayama Ryoko
  中山 亮子
   所属   鶴見大学  歯学部 歯学科 病理学
   職種   助教
論文種別 【査読あり】 研究論文(学術雑誌)
言語種別 英語
査読の有無 査読あり
表題 Aryl Hydrocarbon Receptor-Mediated Induction of EBV Reactivation as a Risk Factor for Sjogren's Syndrome
掲載誌名 正式名:The Journal of Immunology
ISSNコード:00221767
出版社 AMER ASSOC IMMUNOLOGISTS
巻・号・頁 188(9),pp.4654-4662
著者・共著者 Inoue, H.,Mishima, K.,Yamamoto-Yoshida, S.,Ushikoshi-Nakayama, R.,Nakagawa, Y.,Yamamoto, K.,Ryo, K.,Ide, F.,Saito, I.
発行年月 2012/05
概要 The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that mediates a variety of biological effects by binding to environmental pollutants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin). Although numerous animal studies have demonstrated the harmful effects of dioxins, it remains controversial whether dioxins pose a risk to human health. Enhanced lytic replication of EBV is a risk factor for the development of autoimmune diseases and cancers. This study evaluated the possibility that ligand-activated AhR reactivates EBV. EBV reactivation and AhR transactivation were evaluated with luciferase assays. Saliva samples were collected from 19 patients with primary Sjogren's syndrome (SS). Control saliva samples were obtained from 10 healthy individuals and nine patients with severe dry mouth. TCDD enhanced BZLF1 transcription, which mediates the switch from the latent to the lytic form of EBV infection in EBV-positive B cell lines and in a salivary gland epithelial cell line. Moreover, TCDD-induced increases in BZLF1 mRNA and EBV genomic DNA levels were confirmed in the B cell lines. Saliva from SS patients activated the transcription of both CYP
DOI 10.4049/jimmunol.1101575
PMID 22467650
PermalinkURL http://www.jimmunol.org/content/188/9/4654.long