論文

査読有り
2001年

Interleukin-2-dependent but not independent T-cell lines infected with human T-cell leukemia virus type 1 selectively express CD45RO, a marker for persistent infection in vivo

VIRUS GENES
  • H Moro
  • K Iwai
  • N Mori
  • M Watanabe
  • M Fukushi
  • M Oie
  • M Arai
  • Y Tanaka
  • T Miyawaki
  • F Gejyo
  • M Arakawa
  • M Fujii
  • 全て表示

23
3
開始ページ
263
終了ページ
271
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1023/A:1012565105098
出版者・発行元
KLUWER ACADEMIC PUBL

Human T-cell leukemia virus type 1 (HTLV-1) is an etiologic agent of adult T-cell leukemia. HTLV-1 is exclusively detected in CD45RO+ T-cells in infected individuals, but CD45RO is weakly expressed in HTLV-1-transformed T-cell lines in vitro. The aim of this study was to investigate the role of CD45RO in the persistent HTLV-1 infection in vivo. Flow cytometry showed that only two out of eight interleukin(IL)-2-independent HTLV-1-transformed T-cell lines expressed CD45RO, whereas all five IL-2-dependent ones expressed CD45RO, and the level of expression was higher in IL-2-dependent than in IL-2-independent cells. The high CD45RO expression in IL-2-dependent cell lines was not due to IL-2, since IL-2 had little effect on the expression of CD45RO in T-cell lines. Using western blotting, we showed that IL-2-dependent HTLV-1-transformed T-cell lines expressed a lower level of expression of the viral transcriptional regulatory protein Tax than IL-2-independent ones, and that the level of expression correlated inversely with that of CD45RO. However, the expression of Tax in one HTLV-1-negative T-cell line little affected the expression of CD45RO, suggesting that Tax at least alone does not suppress the expression of CD45RO in HTLV-1-infected T-cell lines, and that other viral or cellular factor(s) are probably involved in such suppression. Our results suggest that CD45RO+ Tax-low IL-2-dependent T-cell lines in vitro correspond to the persistent HTLV-1-infected cells in vivo, and HTLV-1-infected cells in vivo are immortalized in IL-2-dependent manner.

リンク情報
DOI
https://doi.org/10.1023/A:1012565105098
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/11778694
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000172031600003&DestApp=WOS_CPL
ID情報
  • DOI : 10.1023/A:1012565105098
  • ISSN : 0920-8569
  • PubMed ID : 11778694
  • Web of Science ID : WOS:000172031600003

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