ArticleInternational journal of molecular sciences2014
Galectin-9 induced myeloid suppressor cells expand regulatory T cells in an IL-10-dependent manner in CVB3-induced acute myocarditis.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Galectin-9 in synergy with NF-κB inhibition restores immune regulatory capability in dendritic cells of subjects with food allergy.Clinical and experimental immunology · 2023Article
- The interplay of galectins-1, -3, and -9 in the immune-inflammatory response underlying cardiovascular and metabolic disease.Cardiovascular diabetology · 2022Review
- Galectin-9: From cell biology to complex disease dynamics.Journal of biosciences · 2016Review
- WNT16B from ovarian fibroblasts induces differentiation of regulatory T cells through β-catenin signal in dendritic cells.International journal of molecular sciences · 2014Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of the study was to explore the effects of galectin-9 on myeloid suppressor cells in Coxsackievirus B3 (CVB3)-induced myocarditis and the possible mechanisms involved. For this purpose, BALB/c male mice were infected with CVB3 on day 0 and then received intraperitoneal (IP) administration of recombinant galectin-9 or phosphate-buffered saline (PBS) daily from day 3 to day 7. The phenotypes and functions of myeloid suppressor cells were evaluated. The role and mechanism of myeloid suppressor cells and subsets in CVB3-induced myocarditis in vitro were explored. We found that galectin-9 remarkably increased the frequencies of CD11b+Gr-1+ cells in the cardiac tissue and spleen with myocarditis. Ly-6G+ cells were decreased and Ly-6C+ cells were increased in galectin-9-treated mice. In addition, CD11b+Gr-1+ cells were highly effective in suppressing CD4+ T cells. Moreover, our data demonstrate that CD11b+Gr-1+ cells are capable of expanding regulatory T cells (Tregs) from a preexisting population of natural Tregs, which depends on IL-10 but not TGF-β. Our results indicate that galectin-9 therapy may represent a useful approach to ameliorate CVB3-induced myocarditis.
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