Galectin-3 deficiency reduces the severity of experimental autoimmune encephalomyelitis

H-R Jiang, Z. Al Rasebi, E. Mensah-Brown, A. Shahin, D. Xu, C.S. Goodyear, S.Y. Fukuda, F.T. Liu, Foo-Yew Liew, Miodrag L Lukic

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154 Citations (Scopus)


Galectin-3 (Gal-3) is a member of the beta-galactoside-binding lectin family and plays an important role in inflammation. However, the precise role of Gal-3 in autoimmune diseases remains obscure. We have investigated the functional role of Gal-3 in experimental autoimmune encephalomyelitis (EAE) following immunization with myelin oligodendrocyte glycoprotein (MOG)35-55 peptide. Gal-3 deficient (Gal-3-/-) mice developed significantly milder EAE and markedly reduced leukocyte infiltration in the CNS compared with similarly treated wild-type (WT) mice. Gal-3-/- mice also contained fewer monocytes and macrophages but more apoptotic cells in the CNS than did WT mice. Following Ag stimulation in vitro, lymph node cells from the immunized Gal-3-/- mice produced less IL-17 and IFN-gamma than did those of the WT mice. In contrast, Gal-3-/- mice produced more serum IL-10, IL-5, and IL-13 and contained higher frequency of Foxp3+ regulatory T cells in the CNS than did the WT mice. Furthermore, bone marrow-derived dendritic cells from Gal-3-/- mice produced more IL-10 in response to LPS or bacterial lipoprotein than did WT marrow-derived dendritic cells. Moreover, Gal-3-/- dendritic cells induced Ag-specific T cells to produce more IL-10, IL-5, and IL-12, but less IL-17, than did WT dendritic cells. Taken together, our data demonstrate that Gal-3 plays an important disease-exacerbating role in EAE through its multifunctional roles in preventing cell apoptosis and increasing IL-17 and IFN-gamma synthesis, but decreasing IL-10 production.
Original languageEnglish
Pages (from-to)1167-1173
Number of pages7
JournalJournal of Immunology
Issue number2
Publication statusPublished - 15 Jan 2009


  • animals
  • apoptosis
  • cells
  • cultured
  • central nervous system
  • down-regulation/immunology
  • encephalomyelitis
  • autoimmune
  • galectin 3
  • glycoproteins
  • growth inhibitors
  • interleukin-10
  • male
  • mice
  • peptide fragments


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