title: Galectin-9 induced myeloid suppressor cells expand regulatory T cells in an IL-10-dependent manner in CVB3-induced acute myocarditis.
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.
authors.affiliation: Laboratory of Medicine of The First Affiliated Hospital, Wannan Medical College, 2 Western Zheshan Road, Wuhu 241001, China. ying-micky@163.com.
authors.forename: Yingying
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Pharmacy, Institute of Dermatology, Chinese Academy of Medical Sciences, Nanjing 210001, China. jiangli718@aliyun.com.
authors.forename: Li
authors.initials: L
authors.lastname: Jiang
authors.affiliation: Central Laboratory of The First Affiliated Hospital, Wannan Medical College, 2 Western Zheshan Road, Wuhu 241001, China. zhangmy1983@163.com.
authors.forename: Mengying
authors.initials: M
authors.lastname: Zhang
authors.affiliation: Central Laboratory of The First Affiliated Hospital, Wannan Medical College, 2 Western Zheshan Road, Wuhu 241001, China. lvkun315@gmail.com.
authors.forename: Kun
authors.initials: K
authors.lastname: Lv
mesh_terms: D000208:Acute Disease; D000818:Animals; D039481:CD11b Antigen / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D018920:Coculture Techniques; D029822:Enterovirus B, Human / Q000502:physiology; D005434:Flow Cytometry; D037161:Galectins / Q000008:administration & dosage / Q000235:genetics / Q000494:pharmacology*; D054884:Host-Pathogen Interactions / Q000187:drug effects; D006801:Humans; D016753:Interleukin-10 / Q000378:metabolism*; D008297:Male; D008807:Mice, Inbred BALB C; D022423:Myeloid Cells / Q000187:drug effects* / Q000378:metabolism; D009205:Myocarditis / Q000378:metabolism / Q000517:prevention & control* / Q000821:virology; D019707:Receptors, Chemokine / Q000378:metabolism; D011994:Recombinant Proteins / Q000235:genetics / Q000494:pharmacology; D016019:Survival Analysis; D013601:T-Lymphocytes / Q000187:drug effects / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects* / Q000378:metabolism
chemical_list: D039481:CD11b Antigen; D037161:Galectins; C503133:Gr-1 protein, mouse; D019707:Receptors, Chemokine; D011994:Recombinant Proteins; C508186:galectin 9, mouse; D016753:Interleukin-10