論文

査読有り 筆頭著者
2007年7月

Crosstalk between RANKL and Fas signaling in dendritic cells controls immune tolerance

BLOOD
  • Takashi Izawa
  • ,
  • Naozurni Ishimaru
  • ,
  • Keiji Moriyama
  • ,
  • Masayuki Kohashi
  • ,
  • Rieko Arakaki
  • ,
  • Yoshio Hayashi

110
1
開始ページ
242
終了ページ
250
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1182/blood-2006-11-059980
出版者・発行元
AMER SOC HEMATOLOGY

Although receptor activator of nuclear factor (NF)-kappa B ligand (RANKL) signaling has been shown to prolong the survival of mature dendritic cells (DCs), the association of RANKL pathway with Fas-mediated apoptosis is obscure. Here, we found that bone marrow-derived DCs (BMDCs) from the Fas-deficient strain MRL/lpr mice, could survive much longer than normal DCs. The expressions of Bcl-x and Bcl-2 and the nuclear transport of NF-kappa B of RANKL-stimulated BMDCs from MRL/lpr mice were significantly upregulated. By contrast, Fas expression of BMDCs from normal C57BL/6 and MRL+/+ mice was increased by RANKL stimulation, and an enhanced DC apoptosis was found when stimulated with both RANKL and anti-Fas mAb, which was associated with activation of caspase-3 and caspase-9. Furthermore, the expression of FLIPL, an inhibitory molecule against Fas-mediated apoptosis, in normal DCs was significantly decreased by RANKL and anti-Fas mAb. Indeed, the adoptive transfer of RANKL-stimulated DCs resulted in rapid acceleration of autoimmunity in MRL/lpr recipients. These findings indicate that the crosstalk between RANKL and Fas signaling in DCs might control immune tolerance.

リンク情報
DOI
https://doi.org/10.1182/blood-2006-11-059980
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/17371940
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000247611000037&DestApp=WOS_CPL
ID情報
  • DOI : 10.1182/blood-2006-11-059980
  • ISSN : 0006-4971
  • PubMed ID : 17371940
  • Web of Science ID : WOS:000247611000037

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