論文

査読有り
2005年10月

The uptake and degradation of DNA is impaired in macrophages and dendritic cells from NZB/W F-1 mice

IMMUNOLOGY LETTERS
  • Y Ogawa
  • ,
  • T Yoshinaga
  • ,
  • K Yasuda
  • ,
  • M Nishikawa
  • ,
  • Y Takakura

101
1
開始ページ
32
終了ページ
40
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.imlet.2005.05.003
出版者・発行元
ELSEVIER SCIENCE BV

DNA/anti-DNA Ab immune complexes seem to play the critical roles in the development of systemic lupus erythematosus (SLE). However, little is known about the removal of DNA by M Phi and DC. We found that elicited peritoneal M Phi s and BM-derived DCs from a lupus-prone strain of New Zealand Black/White F-1 (NZB/W) mice showed impaired DNA uptake and degradation compared with those from control ICR mice. The impairment was mainly observed as the reduced degradation of DNA probably in endosomal compartment and this impaired DNA degradation might, at least in part, result from the reduced DNA uptake in these phagocytic cells. In addition, these impairments was not related to the disease progression since the cells from diseased, 6-month-old NZB/W mice as well as the cells from prediseased, 5-week-old NZB/W mice also exhibited the similar impairment. We also found that the M Phi s and DCs of diseased NZB/W mice showed reduced DNA binding at 4 degrees C. However, this reduced DNA binding could be restored to the control level by pretreatment with DNase. Interestingly, this pretreatment had little effect on the DNA uptake in M Phi s and DCs of diseased NZB/W mice at 37 degrees C. Hence, the present results imply an impaired function of lupus M Phi s and DCs of NZB/W mice to cause retained DNA clearance. (c) 2005 Elsevier B.V. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.imlet.2005.05.003
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/15979158
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000232480400005&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.imlet.2005.05.003
  • ISSN : 0165-2478
  • PubMed ID : 15979158
  • Web of Science ID : WOS:000232480400005

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