論文

査読有り
2012年1月

Size-Dependent Attenuation of TLR9 Signaling by Gold Nanoparticles in Macrophages

JOURNAL OF IMMUNOLOGY
  • Chiau-Yuang Tsai
  • ,
  • Shiou-Ling Lu
  • ,
  • Chia-Wen Hu
  • ,
  • Chen-Sheng Yeh
  • ,
  • Gwo-Bin Lee
  • ,
  • Huan-Yao Lei

188
1
開始ページ
68
終了ページ
76
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.4049/jimmunol.1100344
出版者・発行元
AMER ASSOC IMMUNOLOGISTS

Gold nanoparticles (GNPs), which are generally thought to be bio-inert and non-cytotoxic, have become one of the most ideal nanomaterials for medical applications. Once engulfed by phagocytes, the immunological effects of GNPs are still of concern and require detailed investigation. Therefore, this study explored the immunological significance of GNPs on TLR-mediated innate immunity in murine macrophages. GNP causes specific inhibition of TLR9 (CpG oligodeoxynucleotides; CpG-ODNs) signal in macrophages. The impaired CpG-ODN-induced TNF-alpha production is GNP concentration-and size-dependent in murine Raw264.7 cells: a GNP of 4 nm in size is more potent than a GNP of 11, 19, 35, or 45 nm in size. Consistent with cytokine inhibition, the CpG-ODN-induced phosphorylation of NF-kappa B and JNK as well as NF-kappa B activation are suppressed by GNPs. GNPs accumulate in lysosomes after phagocytosis and also increase TLR9-associated lysosomal cathepsin expression and activities, but this is irrelevant to TLR9 inhibition by GNPs in our studies. In addition, GNPs affected TLR9 translocation in response to CpG-ODNs and to phagosomes. Further exploring how GNPs inhibited TLR9 function, we found that GNPs could bind to high-mobility group box-1 (which is involved in the regulation of TLR9 signaling) inside the lysosomes. The current studies demonstrate that size-dependent inhibition of TLR9 function by GNP may be attributed to its binding to high-mobility group box-1. The Journal of Immunology, 2012, 188: 68-76.

Web of Science ® 被引用回数 : 118

リンク情報
DOI
https://doi.org/10.4049/jimmunol.1100344
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000298628400012&DestApp=WOS_CPL
ID情報
  • DOI : 10.4049/jimmunol.1100344
  • ISSN : 0022-1767
  • eISSN : 1550-6606
  • Web of Science ID : WOS:000298628400012

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