Human T lymphotropic virus-1 infection of human T lymphocytes induces expression of the β-galactoside-binding lectin, galectin-3

Daniel K. Hsu, Stephen R. Hammes, Ichiro Kuwabara, Warner C. Greene, Fu-Tong Liu

Research output: Contribution to journalArticle

119 Citations (Scopus)

Abstract

Animal lectins play important roles in a variety of biological processes via their recognition of glycoconjugates. Galectin-3 is a β-galactoside-binding lectin previously designated as εBP (IgE-binding protein), CBP35, Mac-2, L-29, and L-34, and its expression has been associated with various physiological and pathological processes, including cell growth, tumor transformation, and metastasis. Galectin-3 is widely distributed in various tissues and cell types and is expressed in many leukocytes, with the notable exception of B and T lymphocytes. We now report that galectin-3 is abundantly expressed in a number of human T lymphotropic virus (HTLV)-I-infected human T cell lines, including F6T, HUT 102, K3T, MT-2, and SLB-I, but is not expressed in non-HTLV-I-infected T cell lines such as Jurkat, CEM, and MOLT-4. In addition, the galectin-3 level was markedly increased in human thymocytes after infection with HTLV-I as compared with uninfected thymocytes. The up-regulation of galectin-3 expression appeared to correlate well with HTLV-I gene expression, as undetectable or very low levels of galectin-3 were found in the S1T and ATL-1K cell lines, which are nonproductively infected with HTLV-I. In co-transfection experiments, the galectin-3 promoter was significantly up-regulated by expression vectors encoding the 40-kd Tax protein, a potent transactivator in HTLV-I. Analysis of various Tax mutants suggested that galectin-3 promoter induction is dependent on activation of the cyclic-AMP-responsive element binding protein/activation transcription factor family of transcription factors and, to a lesser extent, nuclear factor-κB/ Rel induction. Transfection of human promonocytic U-937 cells with an HTLV-I Tax expression vector induced galectin-3 expression in this cell line. Functionally, galectin-3 was shown to activate interleukin-2 production in Jurkat T cells. Together, these findings raise the possibility that HTLV-I Tax production induces the transcription and subsequent synthesis and secretion of galectin-3, which in turn may further activate these T cells and contribute to the altered properties of cell growth found in adult T cell leukemia induced by HTLV-I.

Original languageEnglish (US)
Pages (from-to)1661-1670
Number of pages10
JournalAmerican Journal of Pathology
Volume148
Issue number5
StatePublished - May 1996

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Galectin 3
Galactosides
Human T-lymphotropic virus 1
Virus Diseases
Lectins
T-Lymphocytes
Viruses
Cell Line
Thymocytes
Transfection
Transcription Factors
tax Gene Products
Physiological Phenomena
Biological Phenomena
Adult T Cell Leukemia Lymphoma
Glycoconjugates
Jurkat Cells
Trans-Activators
Pathologic Processes
Growth

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Human T lymphotropic virus-1 infection of human T lymphocytes induces expression of the β-galactoside-binding lectin, galectin-3. / Hsu, Daniel K.; Hammes, Stephen R.; Kuwabara, Ichiro; Greene, Warner C.; Liu, Fu-Tong.

In: American Journal of Pathology, Vol. 148, No. 5, 05.1996, p. 1661-1670.

Research output: Contribution to journalArticle

Hsu, Daniel K. ; Hammes, Stephen R. ; Kuwabara, Ichiro ; Greene, Warner C. ; Liu, Fu-Tong. / Human T lymphotropic virus-1 infection of human T lymphocytes induces expression of the β-galactoside-binding lectin, galectin-3. In: American Journal of Pathology. 1996 ; Vol. 148, No. 5. pp. 1661-1670.
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abstract = "Animal lectins play important roles in a variety of biological processes via their recognition of glycoconjugates. Galectin-3 is a β-galactoside-binding lectin previously designated as εBP (IgE-binding protein), CBP35, Mac-2, L-29, and L-34, and its expression has been associated with various physiological and pathological processes, including cell growth, tumor transformation, and metastasis. Galectin-3 is widely distributed in various tissues and cell types and is expressed in many leukocytes, with the notable exception of B and T lymphocytes. We now report that galectin-3 is abundantly expressed in a number of human T lymphotropic virus (HTLV)-I-infected human T cell lines, including F6T, HUT 102, K3T, MT-2, and SLB-I, but is not expressed in non-HTLV-I-infected T cell lines such as Jurkat, CEM, and MOLT-4. In addition, the galectin-3 level was markedly increased in human thymocytes after infection with HTLV-I as compared with uninfected thymocytes. The up-regulation of galectin-3 expression appeared to correlate well with HTLV-I gene expression, as undetectable or very low levels of galectin-3 were found in the S1T and ATL-1K cell lines, which are nonproductively infected with HTLV-I. In co-transfection experiments, the galectin-3 promoter was significantly up-regulated by expression vectors encoding the 40-kd Tax protein, a potent transactivator in HTLV-I. Analysis of various Tax mutants suggested that galectin-3 promoter induction is dependent on activation of the cyclic-AMP-responsive element binding protein/activation transcription factor family of transcription factors and, to a lesser extent, nuclear factor-κB/ Rel induction. Transfection of human promonocytic U-937 cells with an HTLV-I Tax expression vector induced galectin-3 expression in this cell line. Functionally, galectin-3 was shown to activate interleukin-2 production in Jurkat T cells. Together, these findings raise the possibility that HTLV-I Tax production induces the transcription and subsequent synthesis and secretion of galectin-3, which in turn may further activate these T cells and contribute to the altered properties of cell growth found in adult T cell leukemia induced by HTLV-I.",
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T1 - Human T lymphotropic virus-1 infection of human T lymphocytes induces expression of the β-galactoside-binding lectin, galectin-3

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AU - Hammes, Stephen R.

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AU - Greene, Warner C.

AU - Liu, Fu-Tong

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