Elevated expression of CCL5/RANTES in adult T-cell leukemia cells: Possible transactivation of the CCL5 gene by human T-cell leukemia virus type I tax

Naoki Mori*, Alan M. Krensky, Koichi Ohshima, Mariko Tomita, Takehiro Matsuda, Takao Ohta, Yasuaki Yamada, Masao Tomonaga, Shuichi Ikeda, Naoki Yamamoto

*Corresponding author for this work

Research output: Contribution to journalArticle

30 Scopus citations

Abstract

HTLV-I is the etiologic agent of ATL and of tropical spastic paraparesis/HTLV-I-associated myelopathy. Infiltration of various tissues by circulating leukemic cells and HTLV-I-infected T cells is a characteristic of ATL and HTLV-I-associated inflammatory diseases. Chemokines play important roles in migration and tissue localization of various lymphocyte subsets. Here, we report the highly frequent expression of CCL5 (RANTES) in ATL and HTLV-I-infected T-cell lines. Among various human T-cell lines, those infected with HTLV-I selectively expressed the CCL5 gene and secreted CCL5. Furthermore, CCL5 was expressed by leukemic cells in peripheral blood and lymph nodes from patients with ATL. Inducible expression of HTLV-I transcriptional activator Tax in a human T-cell line Jurkat, up-regulated CCL5 mRNA and induced CCL5 secretion. Analysis of the CCL5 promoter revealed that this gene is activated by Tax, via the activation of NF-κB, whose responsive element, R(A/B), is located at positions -71 to -43 relative to the putative transcription start site. Aberrant expression of CCL5 by HTLV-I-infected T cells may impact on the pathophysiology of HTLV-I-associated diseases.

Original languageEnglish (US)
Pages (from-to)548-557
Number of pages10
JournalInternational Journal of Cancer
Volume111
Issue number4
DOIs
StatePublished - Sep 10 2004

Keywords

  • ATL
  • CCL5
  • HTLV-I
  • NF-κB
  • Tax

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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