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Blood, Vol. 93 No. 7 (April 1), 1999:
pp. 2360-2368
Constitutive Activation of NF- B in Primary Adult T-Cell Leukemia
Cells
Naoki Mori,
Masahiro Fujii,
Shuichi Ikeda,
Yasuaki Yamada,
Masao Tomonaga,
Dean W. Ballard, and
Naoki Yamamoto
From the Department of Preventive Medicine and AIDS Research,
Research Field of Pathogenesis and Clinical Sciences, Institute of
Tropical Medicine, Nagasaki University, the Department of Laboratory
Medicine, Nagasaki University School of Medicine, the Department of
Hematology, Atomic Disease Institute, Nagasaki University School of
Medicine, Nagasaki; the Department of Medicine, City of Sasebo General
Hospital, Sasebo; the Department of Virology, Niigata University School
of Medicine, Niigata, Japan; and Howard Hughes Medical Institute,
Vanderbilt University School of Medicine, Nashville, TN.
Human T-cell leukemia virus type I (HTLV-I) is an
etiologic agent of adult T-cell leukemia (ATL). The viral protein Tax
induces the activation and nuclear translocalization of transcription factor NF- B, which is proposed to play a crucial role in the transformation of T cells by HTLV-I. However, the HTLV-I genes including Tax are not expressed significantly in primary leukemic cells
from ATL patients. In this study, we examined the basis for NF-B
activation in freshly isolated leukemic cells from ATL patients. We
found that leukemic cells from ATL patients, like HTLV-I-infected
T-cell lines, display constitutive NF-B DNA binding activity and
increased degradation of IB (an inhibitor of NF-B). Whereas
the NF-B binding activity in Tax-expressing T-cell lines consisted
mostly of p50/c-Rel, fresh ATL samples contained p50/p50 and p50/p65
heterodimers. One T-cell line derived from ATL leukemic cells, TL-Om1,
displayed constitutive NF-B activity, as well as enhanced
degradation of IB, despite the lack of detectable Tax expression.
Interestingly, the NF-B in TL-Om1 consists of p50/p50 and p50/p65
like that in fresh primary leukemic cells. Our results suggest that
activation of NF-B occurs through a Tax-independent mechanism in
leukemic cells of ATL patients, possibly due to differential NF-B
subunit activation.
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