Galectin-9 suppresses Th17 cell development in an IL-2-dependent but Tim-3-independent manner

Clin Immunol. 2012 Apr;143(1):51-8. doi: 10.1016/j.clim.2012.01.004. Epub 2012 Jan 17.

Abstract

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-β1 and IL-6, exogenous Gal-9 suppressed Th17 cell development and expanded Foxp3(+) Tregs from naïve 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-α-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 β-galactosides that suppress Th17 development.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylgalactosamine / analogs & derivatives
  • Acetylgalactosamine / pharmacology
  • Animals
  • Benzyl Compounds / pharmacology
  • Cells, Cultured
  • Encephalomyelitis, Autoimmune, Experimental / genetics
  • Encephalomyelitis, Autoimmune, Experimental / immunology
  • Encephalomyelitis, Autoimmune, Experimental / metabolism
  • Female
  • Flow Cytometry
  • Forkhead Transcription Factors / immunology
  • Forkhead Transcription Factors / metabolism
  • Galectins / genetics
  • Galectins / immunology*
  • Galectins / metabolism
  • Hepatitis A Virus Cellular Receptor 2
  • Interleukin-17 / immunology
  • Interleukin-17 / metabolism
  • Interleukin-2 / immunology*
  • Interleukin-2 / metabolism
  • Interleukin-2 Receptor alpha Subunit / immunology
  • Interleukin-2 Receptor alpha Subunit / metabolism
  • Interleukin-6 / pharmacology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Receptors, Virus / immunology*
  • Receptors, Virus / metabolism
  • T-Lymphocytes, Regulatory / immunology
  • T-Lymphocytes, Regulatory / metabolism
  • Th17 Cells / drug effects
  • Th17 Cells / immunology*
  • Th17 Cells / metabolism
  • Transforming Growth Factor beta1 / pharmacology

Substances

  • Benzyl Compounds
  • Forkhead Transcription Factors
  • Foxp3 protein, mouse
  • Galectins
  • Havcr2 protein, mouse
  • Hepatitis A Virus Cellular Receptor 2
  • Interleukin-17
  • Interleukin-2
  • Interleukin-2 Receptor alpha Subunit
  • Interleukin-6
  • Receptors, Virus
  • Transforming Growth Factor beta1
  • galectin 9, mouse
  • benzyl-alpha-N-acetylgalactosamine
  • Acetylgalactosamine