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Laboratory of Biologic Cancer Therapy, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri
Correspondence: Dr. Peter S. Goedegebuure, Department of Surgery, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, MO 63110. E-mail: goedegep{at}msnotes.wustl.edu
A soluble beta-galactoside-binding lectin, galectin-3 has been shown to
be involved in cell adhesion and activation of immune cells. Although
galectin-3 is known to be expressed in various types of cells, it has
not been shown whether galectin-3 is expressed in T lymphocytes. We
present evidence here that galectin-3 is expressed in activated murine
T lymphocytes including CD4+ and CD8+ T cells
but not in resting T cells. Galectin-3 expression was induced by
anti-CD3 mAb or mitogen and enhanced by common
-chain signaling
cytokines, IL-2, IL-4, and IL-7, in activated T lymphocytes, whereas
the inflammatory cytokines including TNF-
and IFN-
did not.
Galectin-3 expression and proliferation were down-regulated by
withdrawal of IL-2 and gamma irradiation. Anti-sense but not sense
phosphorothioated oligonucleotides for galectin-3 inhibited galectin-3
expression and blocked proliferation of T cells significantly. This
study suggests that up-regulation of galectin-3 plays an important role
in proliferation of activated T lymphocytes.
Key Words: common
-chain signaling cytokines proliferation anti-sense
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