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Blood, Vol. 95 No. 4 (February 15), 2000:
pp. 1420-1426
Thioredoxin prolongs survival of B-type chronic lymphocytic
leukemia cells
Joacim Nilsson,
Ola Söderberg,
Kenneth Nilsson, and
Anders Rosén
From the Department of Biomedicine and Surgery, Division of Cell
Biology, University of Linköping, Sweden; Department of
Pathology, Laboratory of Tumor Biology, University Hospital, Uppsala,
Sweden; Institute for Pathology and Molecular Immunology, University of
Porto, Portugal.
Thioredoxin (Trx) is a ubiquitous protein disulfide oxidoreductase
with antioxidant, cytokine, and chemotactic properties. Previously, we
showed that Trx, in synergy with interleukin 1 (IL-1), IL-2, IL-4,
tumor necrosis factor  (TNF-), and CD40-ligation induced S-phase
entry and mitosis in normal B cells and B-type chronic lymphocytic
leukemia (B-CLL) cells. The viability of B-CLL cells stimulated by
these protocols is high, and it has been hypothesized that the
overexpression of Bcl-2 found in B-CLL protects the cells from
apoptosis in vitro and in vivo. In this study, we have analyzed the
response of cells derived from 12 samples of patients with B-CLL to
recombinant human Trx in spontaneous apoptosis, with special reference
to the Bcl-2 expression. Long-term cultures of B-CLL clones showed
significantly higher viability when supplemented with human Trx
(P = .031), also exemplified with clones surviving more
than 2 months. Short-term cultures of B-CLL cells exposed to 1 µg/mL
of Trx for 1, 5, or 12 days maintained expression or delayed
down-regulation of Bcl-2 compared with control cultures containing RPMI
1640 medium and 10% fetal calf serum only (P = .032, .002, .026, respectively). All B-CLL cells expressed constitutive Trx at
varying but low levels, in contrast to adult T-cell leukemias, which
overexpress Trx, as previously reported. We found that Trx added to
B-CLL cells increased in a dose-dependent fashion the release of
TNF-, which has been suggested to be an autocrine growth factor for
these cells. In conclusion, we have found that human recombinant Trx
induced TNF- secretion, maintained Bcl-2, and reduced apoptosis in
B-CLL cells.
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