Galectin-9 is Involved in Immunosuppression Mediated by Human Bone Marrow-derived Clonal Mesenchymal Stem Cells.
- Author:
Si Na KIM
1
;
Hyun Joo LEE
;
Myung Shin JEON
;
Tacghee YI
;
Sun U SONG
Author Information
- Publication Type:In Vitro ; Original Article
- Keywords: Human mesenchymal stem cells; Immunosuppression; Galectin-9; Apoptosis; TIM-3
- MeSH: Adaptive Immunity; Apoptosis; Cell Death; Cytokines; Galectins; Humans*; Immunosuppression*; Lymphocytes; Mesenchymal Stromal Cells*
- From:Immune Network 2015;15(5):241-251
- CountryRepublic of Korea
- Language:English
- Abstract: Bone marrow-derived mesenchymal stem cells (MSCs) have immunomodulatory properties and can suppress exaggerated pro-inflammatory immune responses. Although the exact mechanisms remain unclear, a variety of soluble factors are known to contribute to MSC-mediated immunosuppression. However, functional redundancy in the immunosuppressive properties of MSCs indicates that other uncharacterized factors could be involved. Galectin-9, a member of the beta-galactoside binding galectin family, has emerged as an important regulator of innate and adaptive immunity. We examined whether galectin-9 contributes to MSC-mediated immunosuppression. Galectin-9 was strongly induced and secreted from human MSCs upon stimulation with pro-inflammatory cytokines. An in vitro immunosuppression assay using a knockdown approach revealed that galectin-9-deficient MSCs do not exert immunosuppressive activity. We also provided evidence that galectin-9 may contribute to MSC-mediated immunosuppression by binding to its receptor, TIM-3, expressed on activated lymphocytes, leading to apoptotic cell death of activated lymphocytes. Taken together, our findings demonstrate that galectin-9 is involved in MSC-mediated immunosuppression and represents a potential therapeutic factor for the treatment of inflammatory diseases.
