Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/11136
Title: Galectin-3 deficiency enhances type 2 immune cell-mediated myocarditis in mice
Authors: Miletic Kovacevic, Marina
Pejnović, Nada
Mitrovic O.
Jovicic, Nemanja
Petrović, Ivica
Arsenijevic, Nebojsa
Lukic, Miodrag
Ljujic, Biljana
Journal: Immunologic Research
Issue Date: 1-Aug-2018
Abstract: © 2018, Springer Science+Business Media, LLC, part of Springer Nature. Experimental autoimmune myocarditis (EAM) is a mouse model of immune-mediated myocarditis and cardiomyopathy. The role of Galectin-3 (Gal-3), a β-galactoside-binding lectin, in autoimmune myocarditis has not been studied. Therefore, the aim of this study was to delineate the role of Gal-3 in myosin peptide-induced autoimmune myocarditis in mice. EAM was induced in relatively resistant C57BL/6J mice (wild type, WT) and in mice with a targeted deletion of Gal-3 gene (Gal-3KO) by immunization with myosin peptide MyHCα334–352. Gal-3KO mice developed more severe myocarditis and more pronounced heart hypertrophy than WT mice. Increased infiltration of CD45+ leucocytes, CD3+ T cells, F4/80+ macrophages, and eosinophils was observed in hearts of Gal-3KO mice compared to WT mice on day 21 after EAM induction. Moreover, hearts of Gal-3KO mice had more T helper type 2 (Th2) cells, alternatively activated M2 macrophages, higher amounts of IgG deposits, and higher serum levels of IL-4 and IL-33 than WT mice. Ablation of Gal-3 in Th1-dominant C57BL/6J mice that are relatively resistant to EAM resulted in more severe disease characterized by type 2 cardiac inflammation. The complex effects of Gal-3 on EAM progression might be important in the consideration of therapeutic options for the treatment of EAM.
URI: https://scidar.kg.ac.rs/handle/123456789/11136
Type: article
DOI: 10.1007/s12026-018-9013-8
ISSN: 0257277X
SCOPUS: 85051553400
Appears in Collections:Faculty of Medical Sciences, Kragujevac

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