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Title: Gal-3 regulates the capacity of dendritic cells to promote NKT-cell-induced liver injury
Authors: Volarevic, Vladislav
Simovic Markovic, Bojana
Bojic, Sanja
Stojanovic, Maja
Nilsson U.
Leffler, Hakon
Besra, Gurdyal
Arsenijevic, Nebojsa
Paunovic, Verica
Trajkovic, Vladimir
Lukic, Miodrag
Journal: European Journal of Immunology
Issue Date: 1-Jan-2015
Abstract: © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. Galectin-3 (Gal-3), an endogenous lectin, exhibits pro- and anti-inflammatory effects in various disease conditions. In order to explore the role of Gal-3 in NKT-cell-dependent pathology, we induced hepatitis in C57BL/6 WT and Gal-3-deficient mice by using specific ligand for NKT cells: α-galactosylceramide, glycolipid Ag presented by CD1d. The injection of α-galactosylceramide significantly enhanced expression of Gal-3 in liver NKT and dendritic cells (DCs). Genetic deletion or selective inhibition of Gal-3 (induced by Gal-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 downregulated. Genetic deletion or selective inhibition of Gal-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 Gal-3 attenuated the capacity of DCs to support liver damage in the passive transfer experiments and to produce pro-inflammatory cytokines in vitro. Gal-3-deficient DCs failed to optimally stimulate production of pro-inflammatory cytokines in NKT cells, in vitro and in vivo. In conclusion, Gal-3 regulates the capacity of DCs to support NKT-cell-mediated liver injury, playing an important pro-inflammatory role in acute liver injury.
Type: Article
DOI: 10.1002/eji.201444849
ISSN: 00142980
SCOPUS: 84923040035
Appears in Collections:Faculty of Medical Sciences, Kragujevac
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