Journal
CLINICAL IMMUNOLOGY
Volume 143, Issue 1, Pages 51-58Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2012.01.004
Keywords
Galectin-9; Tim-3; Regulation; Th17; Treg; Differentiation
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Funding
- Japan Society for Promotion of Science (JSPS) [20790570, 22590360]
- Ministry of Health, Labor and Welfare
- Kagawa University
- Japanese Ministry of Education, Culture, Sports, Science, and Technology
- Grants-in-Aid for Scientific Research [23256004, 22590958, 22590360, 20790570, 23591438] Funding Source: KAKEN
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Galectin-9 (Gal-9) ameliorates autoimmune reactions by suppressing Th17 cells while augmenting Foxp3(+) regulatory T cells (Tregs). However, the exact mechanism of Gal-9-mediated immune modulation has been elusive. In a MOG-induced experimental allergic encephalomyelitis model using Gal-9(-/-) mice, we observed exacerbated inflammation and an increase in IL-17-producing Th17 cells balanced by a decrease in Foxp3+ Tregs. During in vitro Th17 skewing using TGF-beta 1 and IL-6, exogenous Gal-9 suppressed Th17 cell development and expanded Foxp3(+) Tregs from naive CD4 T cells in an IL-2-dependent manner. Although Gal-9 induced cell death in Tim3-expressing differentiated Th17 cells, Gal-9 suppressed Th17 development in a Tim-3-independent. Benzyl-alpha-GalNAc (an O-glycan biosynthesis inhibitor), but not swainsonine (a complex-type N-glycan biosynthesis inhibitor) abrogated Gal-9-mediated inhibition of Th17 development indicating that there is a linkage between Gal-9 and an unidentified glycoprotein(s) with O-linked beta-galactosides that suppress Th17 development. (C) 2012 Elsevier Inc. All rights reserved.
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