| First Author | Kovacevic MM | Year | 2018 |
| Journal | Immunol Res | Volume | 66 |
| Issue | 4 | Pages | 491-502 |
| PubMed ID | 30099675 | Mgi Jnum | J:311792 |
| Mgi Id | MGI:6780370 | Doi | 10.1007/s12026-018-9013-8 |
| Citation | Kovacevic MM, et al. (2018) Galectin-3 deficiency enhances type 2 immune cell-mediated myocarditis in mice. Immunol Res 66(4):491-502 |
| abstractText | Experimental autoimmune myocarditis (EAM) is a mouse model of immune-mediated myocarditis and cardiomyopathy. The role of Galectin-3 (Gal-3), a beta-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 MyHCalpha334-352. 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. |
