ライ ショウホウ   RAI Shouho
  雷 小峰
   所属   埼玉医科大学  医学部 国際医療センター 皮膚科(皮膚腫瘍科)
   職種   助教
論文種別 学術雑誌(原著)
言語種別 英語
査読の有無 査読あり
表題 Delayed growth of EL4 lymphoma in SR-A-deficient mice is due to upregulation of nitric oxide and interferon-gamma production by tumor-associated macrophages
掲載誌名 正式名:CANCER SCIENCE
ISSNコード:1347-9032
出版社 WILEY-BLACKWELL PUBLISHING, INC
巻・号・頁 100(11),2160-2166頁
著者・共著者 Yoshihiro Komohara,Kenichi Takemura,Xiao Feng Lei,Naomi Sakashita,Mamoru Harada,Hiroshi Suzuki,Tatsuhiko Kodama,Motohiro Takeya
発行年月 2009/11
概要 Class A scavenger receptors (SR-A, CD204) are highly expressed in tumor-associated macrophages (TAM). To investigate the function of SR-A in TAM, wild-type and SR-A-deficient (SR-A-/-) mice were injected with EL4 cells. Although these groups of mice did not differ in the numbers of infiltrating macrophages and lymphocytes and in neovascularization, SR-A-/- mice had delayed growth of EL4 tumors. Expression of inducible nitric oxide (NO) synthase and interferon (IFN)-gamma mRNA increased significantly in tumor tissues from SR-A-/- mice. Engulfment of necrotic EL4 cells induced upregulation of NO and IFN-gamma production by cultured macrophages, and production of NO and IFN-gamma increased in SR-A-/- macrophages in vitro. IFN-beta production by cultured macrophages was also elevated in SR-A-/- macrophages in vitro. These results suggested that the antitumor activity of macrophages increased in SR-A-/- mice because of upregulation of NO and IFN-gamma production. These data indicate an important role of SR-A in regulating TAM function by inhibiting toll-like receptor (TLR)4-IFN-beta signaling. (Cancer Sci 2009); 00: 000-000).
DOI 10.1111/j.1349-7006.2009.01296.x
PMID 19694752