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

Am J Pathol. 1996 May;148(5):1661-70.


Animal lectins play important roles in a variety of biological processes via their recognition of glycoconjugates. Galectin-3 is a beta-galactoside-binding lectin previously designated as epsilon BP (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-kappa B/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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antigens, Differentiation / analysis
  • Antigens, Differentiation / biosynthesis*
  • Antigens, Differentiation / genetics
  • Cell Line
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • Galectin 3
  • Gene Expression Regulation, Viral
  • Gene Products, tax / metabolism
  • Genetic Vectors
  • Human T-lymphotropic virus 1 / genetics
  • Human T-lymphotropic virus 1 / isolation & purification*
  • Human T-lymphotropic virus 1 / physiology
  • Humans
  • NF-kappa B / metabolism
  • Promoter Regions, Genetic
  • T-Lymphocytes / chemistry
  • T-Lymphocytes / metabolism*
  • T-Lymphocytes / virology*
  • Thymus Gland / chemistry
  • Thymus Gland / cytology
  • Thymus Gland / virology
  • Transfection


  • Antigens, Differentiation
  • Cyclic AMP Response Element-Binding Protein
  • Galectin 3
  • Gene Products, tax
  • NF-kappa B