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Journal of Virology, February 1999, p. 1271-1277, Vol. 73, No. 2
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Human T-Cell Leukemia Virus Type 1 Tax Protein Abrogates Interleukin-2 Dependence in a Mouse T-Cell Line

Youichi Iwanaga,1,2 Tomonori Tsukahara,2 Takashi Ohashi,2 Yuetsu Tanaka,3 Masaaki Arai,1,2 Masataka Nakamura,4 Kiyoshi Ohtani,4 Yoshihiro Koya,2 Mari Kannagi,2 Naoki Yamamoto,1 and Masahiro Fujii2,5,*

Department of Microbiology1 and Department of Immunotherapeutics,2 Medical Research Division, and Human Gene Science Center,4 Tokyo Medical and Dental University, Yushima, Bunkyo-ku, Tokyo 113, Department of Biosciences, School of Science, Kitasato University, Kitasato 1-15-1, Sagamihara, Kanagawa 228,3 and Department of Virology, Niigata University School of Medicine, Asahimachi-Dori, Niigata 951-8510,5 Japan

Received 9 July 1998/Accepted 2 November 1998

Human T-cell leukemia virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia. Tax, the viral protein, is thought to be crucial in the development of the disease, since it transforms healthy T cells in vitro and induces tumors in transgenic animals. We examined the effect of Tax activity on the growth of the interleukin-2 (IL-2)-dependent T-cell line CTLL-2. Stable expression of Tax in CTLL-2 transformed cell growth from being IL-2 dependent to IL-2 independent. Tax stimulated transcription through NF-kappa B and the cyclic AMP-responsive element-like sequence in the HTLV-1 promoter. The finding of Tax mutants segregating these two pathways suggested that the NF-kappa B pathway was essential for IL-2-independent growth of CTLL-2 cells while the CRE pathway was unnecessary. However, both pathways were necessary for another transformation-related activity (colony formation in soft agar) of CTLL-2/Tax. Our results show that Tax has at least two distinct activities on T cells, and suggest that Tax plays a crucial role in IL-2-independent T-cell transformation induced by HTLV-1, in addition to its well-known IL-2-dependent cell transformation.

* Corresponding author. Mailing address: Department of Virology, Niigata University School of Medicine, 1-757 Asahimachi-Dori, Niigata 951-8510, Japan. Phone: 81-25-227-2115. Fax: 81-25-227-0763. E-mail: fujiimas{at}med.niigata-u.ac.jp.

Journal of Virology, February 1999, p. 1271-1277, Vol. 73, No. 2
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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