論文

査読有り
2014年6月13日

Attenuation of migration properties of CD4+ T cells from aged mice correlates with decrease in chemokine receptor expression, response to retinoic acid, and RALDH expression compared to young mice

Bioscience, Biotechnology, and Biochemistry
  • Jihyun Park
  • ,
  • Takuya Miyakawa
  • ,
  • Aya Shiokawa
  • ,
  • Haruyo Nakajima-Adachi
  • ,
  • Masaru Tanokura
  • ,
  • Satoshi Hachimura

78
6
開始ページ
976
終了ページ
980
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1080/09168451.2014.910099
出版者・発行元
TAYLOR & FRANCIS LTD

Aging results in attenuation of abilities to mount appropriate immune responses. The influence of aging on CD4(+) T cell migration ability toward chemokines was investigated with young and aged mice. We found functional decline in migration ability toward CCL19 and also decreased CCR7 expression level in antigen-stimulated CD4(+) T cells from aged mice compared with those from young mice. Upon addition of retinoic acid (RA), CD4(+) T cells from aged mice showed decreased CCR9 expression level compared to young mice and the migration ability of CD4(+) T cells from aged mice toward CCL25 was attenuated compared to young mice. We also observed that the expression of RALDH2 mRNA was decreased in mesenteric lymph node dendritic cells from aged mice compared to those from young mice. These results demonstrate that attenuated migration abilities of CD4(+) T cells were observed in aged mice, which correlated with decreased chemokine receptor expression. Furthermore, the reduced production and response to RA by aging may be one of the causes of such attenuated migration abilities in the intestinal immune system.

リンク情報
DOI
https://doi.org/10.1080/09168451.2014.910099
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/25036122
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000340133800009&DestApp=WOS_CPL
ID情報
  • DOI : 10.1080/09168451.2014.910099
  • ISSN : 0916-8451
  • eISSN : 1347-6947
  • PubMed ID : 25036122
  • Web of Science ID : WOS:000340133800009

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