International Immunology, Vol. 14, No. 2, 147-155,
February 2002
© 2002 Japanese Society for Immunology
Human T cell leukemia virus type-I Tax activates human macrophage inflammatory protein-3
/CCL20 gene transcription via the NF-
B pathway
1 Division of Cytokine Signaling, Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Medical Sciences, Nagasaki 852-8523, Japan
2 Department of Hematology, Atomic Disease Institute, Nagasaki University School of Medicine, Nagasaki 852-8523, Japan
Correspondence to: T. Matsuyaama; E-mail: tosim{at}net.nagasaki-u.ac.jp
Infection by human T cell leukemia virus type (HTLV)-I is associated with several diseases, including adult T cell leukemia and HTLV-I-associated myelopathy/tropical spastic paraparesis. Leukocytes are attracted to the sites of inflammation by chemotactic factors. Macrophage inflammatory protein (MIP)-3
/CCL20 is a recently isolated member of the CC subfamily of chemokines and has been proposed as a crucial factor to elicit inflammatory reactions. We now report that endogenous MIP-3 mRNA levels are elevated in HTLV-I-infected T cell lines and in a human T cell line following the induced expression of the HTLV-I-encoded transactivator, Tax. Analysis of the human MIP-3 promoter revealed that this gene is activated by Tax, via the activation of nuclear factor (NF)-
B, whose responsive element, –82-B, is located at a position between –82 and –91 relative to the putative transcription start site. With an electromobility shift assay we further demonstrated that the –82-B element was bound by the Tax-activated p50/p65 heterodimers of NF-B. Expression of the specific receptor of MIP-3, CCR6, was also increased in HTLV-I-infected T cell lines, suggesting an autocrine and/or paracrine mechanism to establish the pathogenesis of HTLV-I-associated diseases.
Keywords: human T cell leukemia virus type-I, Tax, macrophage inflammatory protein-3, NF-B
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