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Blood, Vol. 94 No. 11 (December 1), 1999:
pp. 3847-3854
Inhibition of Caspase Cascade by HTLV-I Tax Through Induction of
NF- B Nuclear Translocation
Atsushi Kawakami,
Tomoki Nakashima,
Hideaki Sakai,
Satoshi Urayama,
Satoshi Yamasaki,
Ayumi Hida,
Masahiko Tsuboi,
Hideki Nakamura,
Hiroaki Ida,
Kiyoshi Migita,
Yojiro Kawabe, and
Katsumi Eguchi
From The First Department of Internal Medicine, and the Department of
Hospital Pharmacy, Nagasaki University School of Medicine; and the
Department of Pharmacology, Nagasaki University, School of Dentistry,
Nagasaki, Japan.
NF- B is required for prevention of apoptosis. We examined the
importance of human T-cell leukemia virus-I (HTLV-I) Tax protein to
stimulate NF-B nuclear translocation, thus preventing apoptosis. Jurkat cells and JPX-9 cells in which the inducible Tax expression plasmid vector was stably transfected were used in the present study.
Both Jurkat and Tax JPX-9 cells had small amounts of
basal nuclear NF-B activity. The addition of NF-B inhibitors
suppressed NF-B nuclear translocation of the cells, thus inducing
apoptosis. Sequential activation of caspases from caspase-8 to
caspase-3 was shown during this process. NF-B nuclear translocation
in JPX-9 cells was stimulated through Tax expression, and both the
activation of caspases and apoptosis induced by NF-B inhibitors were
significantly suppressed in the Tax+ JPX-9 cells. The
expression of Bcl-2, Bax, and Bcl-x was not changed among Jurkat,
Tax JPX-9, and Tax+ JPX-9 cells in the
presence or absence of NF-B inhibitors. X-chromosome-linked inhibitor of apoptosis (XIAP) protein expression in Tax
JPX-9 cells was significantly suppressed by NF-B inhibitors, however, its expression in Tax+ JPX-9 cells was
maintained even by the addition of NF-B inhibitors. Our results
suggest that the activation of NF-B via Tax protein in HTLV-I
infected cells renders the cells resistant to apoptosis. The expression
of anti-apoptotic gene products such as XIAP to suppress caspase
cascade, results in an increase of cytokine production and cell
proliferation; one of the proposed mechanisms that promotes autoimmune
disorders such as Sjögren's syndrome and rheumatoid arthritis
found in HTLV-I seropositive subjects.
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