Galectin-3 in induction of regulatory T cell
Date Issued
2009
Date
2009
Author(s)
Wang, Wei-Le
Abstract
Galectin-3 is a 31kDa protein, which belong to a family of mammalian b-galactoside-binding proteins. Galectin-3 is present intracellularly within nucleus and cytoplasm or secreted via non-classical pathway outside of cell; and it also has been implicated in the inflammatory immune response in autoimmune diseases. Previous studies demonstrated that several members of galectin family are able to suppress the autoimmune disease via mediating the function of Treg cells. However, the role of galectin-3 mediating the regulatory function in T cells is remained to be further elucidated. In order to address this issue, we attempt to investigate whether galectin-3 induces the Tregs in vitro and in vivo. We examine the immuno phenotype and expression of the transcription factor in T cells after administration of galectin-3. We also investigate the suppressive function of Treg cells induced by galectin-3 in immune response in vivo. Our results demonstrated that galectin-3 induce the expression of PD-1 and CTLA-4 on both Jurkat cells and human primary T cells. In addition, the expression of FoxP3 is up-regulated in CD4 T cells and the frequency of CD4+FoxP3+TGF-β+ T cell is higher in response to galectin-3 according to flow cytometry analysis. These finding indicate that galectin-3 induce the generation of FoxP3+ T cells and increase the production of TGF-β in vitro, while induction of FoxP3+ T cells is abolished by adding lactose to block the interaction between galectin-3 and its ligands on T cells. Furthermore, treatment with recombinant galectin-3 induced the FoxP3+ T cells and ameliorated the severity of DSS-induced Inflammatory Bowel Disease (IBD). In conclusion, our finding demonstrates that galectin-3 induces Tregs and ameliorates the severity of DSS-induced colitis. It suggests that galectin-3 is potential for therapeutic immuno modulation via induction of Tregs.
Subjects
FoxP3
PD-1
CTLA-4
DSS
SDGs
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