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Journal of Virology, October 1999, p. 7981-7987, Vol. 73, No. 10
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Induction of Bcl-xL Expression by Human T-Cell Leukemia Virus Type 1 Tax through NF-kappa B in Apoptosis-Resistant T-Cell Transfectants with Tax

Tomonori Tsukahara,1 Mari Kannagi,1,2,* Takashi Ohashi,1 Hirotomo Kato,1 Masaaki Arai,3 Gabriel Nunez,4 Youichi Iwanaga,3 Naoki Yamamoto,3 Kiyoshi Ohtani,5 Masataka Nakamura,5 and Masahiro Fujii6

Department of Immunotherapeutics1 and Department of Molecular Virology,3 Medical Research Division, and Human Gene Sciences Center,5 Tokyo Medical and Dental University, Tokyo 113, CREST, Japan Science and Technology Corporation, Saitama 332,2 and Department of Virology, Niigata University School of Medicine, Niigata 951,6 Japan, and Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 481094

Received 10 February 1999/Accepted 14 June 1999

Human T-cell leukemia virus type 1 (HTLV-1) Tax is thought to play a pivotal role in immortalization of T cells. We have recently shown that the expression of Tax protected the mouse T-cell line CTLL-2 against apoptosis induced by interleukin-2 (IL-2) deprivation and converted its growth from being IL-2 dependent to being IL-2 independent. In this study, we demonstrate that constitutive expression of bcl-xl but not bcl-2, bcl-xs, bak, bad, or bax was associated with apoptosis resistance after IL-2 deprivation in CTLL-2 cells that expressed Tax. Transient-transfection assays showed that bcl-x promoter was transactivated by wild-type Tax. Similar effects were observed in mutant Tax retaining transactivating ability through NF-kappa B. Deletion or substitution of a putative NF-kappa B binding site identified in the bcl-x promoter significantly decreased Tax-induced transactivation. This NF-kappa B-like element was able to form a complex with NF-kappa B family proteins in vitro. Furthermore, Tax-induced transactivation of the bcl-x promoter was also diminished by the mutant Ikappa Balpha , which specifically inhibits NF-kappa B activity. Our findings suggest that constitutive expression of Bcl-xL induced by Tax through the NF-kappa B pathway contributes to the inhibition of apoptosis in CTLL-2 cells after IL-2 deprivation.

* Corresponding author. Mailing address: Department of Immunotherapeutics, Tokyo Medical and Dental University, Medical Research Division, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113, Japan. Phone: 81 (3) 5803-5798. Fax: 81 (3) 5803-0235. E-mail: kann.impt{at}med.tmd.ac.jp.

Journal of Virology, October 1999, p. 7981-7987, Vol. 73, No. 10
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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