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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
Author(s) -
Mori Naoki,
Krensky Alan M.,
Ohshima Koichi,
Tomita Mariko,
Matsuda Takehiro,
Ohta Takao,
Yamada Yasuaki,
Tomonaga Masao,
Ikeda Shuichi,
Yamamoto Naoki
Publication year - 2004
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.20266
Subject(s) - tropical spastic paraparesis , ccl5 , transactivation , jurkat cells , biology , cancer research , chemokine , human t lymphotropic virus 1 , t cell leukemia , t cell , gene expression , leukemia , microbiology and biotechnology , virology , immunology , gene , il 2 receptor , inflammation , myelopathy , immune system , genetics , spinal cord , neuroscience
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. © 2004 Wiley‐Liss, Inc.