Induction of allogenic T-cell hyporesponsiveness by galectin-1-mediated apoptotic and non-apoptotic mechanisms

Cell Death Differ. 2002 Jun;9(6):661-70. doi: 10.1038/sj.cdd.4401009.


Galectin-1, a beta-galactoside-binding protein expressed at sites of T-cell activation and immune privilege, has shown specific immunosuppressive properties. Because of the implications of this protein in T-cell tolerance and its potential use to avoid graft rejection, we investigated the immunosuppressive effects of galectin-1 in the course of the human allogenic T-cell response. Galectin-1 induced a dose- and carbohydrate-dependent inhibition of the allogenic T-cell response. Addition of galectin-1 to alloreactive lymphocytes resulted in significant apoptosis of CD45R0-positive cells. This negative regulatory effect was accompanied by caspase activation, Bcl-2 downregulation and was prevented by addition of exogenous IL-2. In addition, a significant decrease of IFN-gamma production was detected in the non-apoptotic cell population, following exposure of alloreactive lymphocytes to galectin-1. Moreover, the immunosuppressive activity of this protein did not involve TGF-beta-mediated mechanisms. Since galectin-1 is expressed by activated T cells and could be acting by an autocrine negative loop to control human T-cell reactivity, we finally examined the regulated expression of this protein throughout the allogenic T-cell response. Expression of endogenous galectin-1 was detected at 24 h of cell culture, reaching its maximal levels after 72 h of allostimulation. The present study sets the basis for a potential use of galectin-1 as a selective immunosuppressive agent to limit T-cell-mediated reactivity during the effector phase of the alloimmune response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Apoptosis*
  • Carbohydrates / immunology
  • Caspases / metabolism
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Galectin 1 / biosynthesis
  • Galectin 1 / pharmacology*
  • Humans
  • Immunosuppressive Agents / pharmacology*
  • Interferon-gamma / metabolism
  • Interleukin-2 / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism
  • Transforming Growth Factor beta / metabolism


  • Carbohydrates
  • Galectin 1
  • Immunosuppressive Agents
  • Interleukin-2
  • Proto-Oncogene Proteins c-bcl-2
  • Transforming Growth Factor beta
  • Interferon-gamma
  • Caspases