Gal-3 regulates the capacity of dendritic cells to promote NKT cell-induced liver injury

Research output: Contribution to journalArticlepeer-review


  • Vladislav Volarevic
  • Bojana Simovic Markovic
  • Sanja Bojic
  • Maja Stojanovic
  • Ulf Nilsson
  • Hakon Leffler
  • Nebojsa Arsenijevic
  • Verica Paunovic
  • Vladimir Trajkovic
  • Miodrag L Lukic

Colleges, School and Institutes

External organisations

  • Centre for Molecular Medicine and Stem Cell Research, Faculty of Medical Sciences, University of Kragujevac, Kragujevac, Serbia.


Galectin-3, an endogenous lectin, exhibits pro- and anti-inflammatory effects in various disease conditions. In order to explore the role of galectin-3 in NKT cell-dependent pathology, we induced hepatitis in C57BL/6 wild type and galectin-3 deficient mice by using specific ligand for NKT cells: α-galactosylceramide, glycolipid antigen presented by CD1d. The injection of α-galactosylceramide significantly enhanced expression of galectin-3 in liver NKT and dendritic cells (DCs). Genetic deletion or selective inhibition of galectin-3 (induced by galectin-3 inhibitor TD139) abrogated the susceptibility to NKT cell-dependent hepatitis. Blood levels of pro-inflammatory cytokines (TNF-α, IFN-γ, IL-12) and their production by liver DCs and NKT cells were also down-regulated. Genetic deletion or selective inhibition of galectin-3 alleviated influx of inflammatory CD11c+CD11b+ DCs in the liver and favored tolerogenic phenotype and IL-10 production of liver NKT and DCs. Deletion of galectin-3 attenuated capacity of DCs to support liver damage in the passive transfer experiments and to produce pro-inflammatory cytokines in vitro. Galectin-3-deficient DCs failed to optimally stimulate production of pro-inflammatory cytokines in NKT cells, in vitro and in vivo. In conclusion, galectin-3 regulates the capacity of DCs to support NKT cell-mediated liver injury, playing an important pro-inflammatory role in acute liver injury. This article is protected by copyright. All rights reserved.

Bibliographic note

This article is protected by copyright. All rights reserved.


Original languageEnglish
JournalEuropean Journal of Immunology
Publication statusPublished - 31 Oct 2014