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      Galectin-9 suppresses the generation of Th17, promotes the induction of regulatory T cells, and regulates experimental autoimmune arthritis.

      Clinical Immunology (Orlando, Fla.)
      Animals, Arthritis, Experimental, immunology, metabolism, Autoantigens, Autoimmune Diseases, Cell Differentiation, Collagen, Flow Cytometry, Galectins, genetics, Humans, Interferon-gamma, Interleukin-12, Interleukin-17, Male, Mice, Mice, Inbred C57BL, Mice, Inbred DBA, Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, T-Lymphocyte Subsets, cytology, T-Lymphocytes, Helper-Inducer, T-Lymphocytes, Regulatory

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          Abstract

          The effects of galectin-9 on a mouse collagen-induced arthritis (CIA) model were assessed to clarify whether galectin-9 suppresses CIA by regulating T cell immune responses. Galectin-9 suppressed CIA in a dose-dependent manner, and such suppression was observed even when treatment was started on 7 days after the booster, indicating its preventive and therapeutic effects. Galectin-9 induced the decreased levels of pro-inflammatory cytokines, IL-17, IL-12, and IFNgamma in the joint. Galectin-9 induced the decreased number of CD4(+) TIM-3(+) T cells in peripheral blood. Galectin-9-deficient mice became susceptible to CIA may be by increased number of CD4(+) TIM-3(+) T cells and decreased number of Treg cells. We further found that galectin-9 induces differentiation of naive T cells to Treg cells, and it suppresses differentiation to Th17 cells in vitro. The present results suggested that galectin-9 ameliorates CIA by suppressing the generation of Th17, promoting the induction of regulatory T cells.

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