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Galectin-1 is essential for the induction of MOG35-55 -based intravenous tolerance in experimental autoimmune encephalomyelitis.

Publication ,  Journal Article
Mari, ER; Rasouli, J; Ciric, B; Moore, JN; Conejo-Garcia, JR; Rajasagi, N; Zhang, G-X; Rabinovich, GA; Rostami, A
Published in: Eur J Immunol
July 2016

In experimental autoimmune encephalomyelitis (EAE), intravenous (i.v.) injection of the antigen, myelin oligodendrocyte glycoprotein-derived peptide, MOG35-55 , suppresses disease development, a phenomenon called i.v. tolerance. Galectin-1, an endogenous glycan-binding protein, is upregulated during autoimmune neuroinflammation and plays immunoregulatory roles by inducing tolerogenic dendritic cells (DCs) and IL-10 producing regulatory type 1 T (Tr1) cells. To examine the role of galectin-1 in i.v. tolerance, we administered MOG35-55 -i.v. to wild-type (WT) and galectin-1 deficient (Lgals1(-/-) ) mice with ongoing EAE. MOG35-55 suppressed disease in the WT, but not in the Lgals1(-/-) mice. The numbers of Tr1 cells and Treg cells were increased in the CNS and periphery of tolerized WT mice. In contrast, Lgals1(-/-) MOG-i.v. mice had reduced numbers of Tr1 cells and Treg cells in the CNS and periphery, and reduced IL-27, IL-10, and TGF-β1 expression in DCs in the periphery. DCs derived from i.v.-tolerized WT mice suppressed disease when adoptively transferred into mice with ongoing EAE, whereas DCs from Lgals1(-/-) MOG-i.v. mice were not suppressive. These findings demonstrate that galectin-1 is required for i.v. tolerance induction, likely via induction of tolerogenic DCs leading to enhanced development of Tr1 cells, Treg cells, and downregulation of proinflammatory responses.

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Published In

Eur J Immunol

DOI

EISSN

1521-4141

Publication Date

July 2016

Volume

46

Issue

7

Start / End Page

1783 / 1796

Location

Germany

Related Subject Headings

  • T-Lymphocyte Subsets
  • Peptide Fragments
  • Myelin-Oligodendrocyte Glycoprotein
  • Multiple Sclerosis
  • Mice, Knockout
  • Mice
  • Lymphocyte Count
  • Immunophenotyping
  • Immunology
  • Immune Tolerance
 

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Mari, E. R., Rasouli, J., Ciric, B., Moore, J. N., Conejo-Garcia, J. R., Rajasagi, N., … Rostami, A. (2016). Galectin-1 is essential for the induction of MOG35-55 -based intravenous tolerance in experimental autoimmune encephalomyelitis. Eur J Immunol, 46(7), 1783–1796. https://doi.org/10.1002/eji.201546212
Mari, Elisabeth R., Javad Rasouli, Bogoljub Ciric, Jason N. Moore, José R. Conejo-Garcia, Naveen Rajasagi, Guang-Xian Zhang, Gabriel A. Rabinovich, and Abdolmohamad Rostami. “Galectin-1 is essential for the induction of MOG35-55 -based intravenous tolerance in experimental autoimmune encephalomyelitis.Eur J Immunol 46, no. 7 (July 2016): 1783–96. https://doi.org/10.1002/eji.201546212.
Mari ER, Rasouli J, Ciric B, Moore JN, Conejo-Garcia JR, Rajasagi N, et al. Galectin-1 is essential for the induction of MOG35-55 -based intravenous tolerance in experimental autoimmune encephalomyelitis. Eur J Immunol. 2016 Jul;46(7):1783–96.
Mari, Elisabeth R., et al. “Galectin-1 is essential for the induction of MOG35-55 -based intravenous tolerance in experimental autoimmune encephalomyelitis.Eur J Immunol, vol. 46, no. 7, July 2016, pp. 1783–96. Pubmed, doi:10.1002/eji.201546212.
Mari ER, Rasouli J, Ciric B, Moore JN, Conejo-Garcia JR, Rajasagi N, Zhang G-X, Rabinovich GA, Rostami A. Galectin-1 is essential for the induction of MOG35-55 -based intravenous tolerance in experimental autoimmune encephalomyelitis. Eur J Immunol. 2016 Jul;46(7):1783–1796.
Journal cover image

Published In

Eur J Immunol

DOI

EISSN

1521-4141

Publication Date

July 2016

Volume

46

Issue

7

Start / End Page

1783 / 1796

Location

Germany

Related Subject Headings

  • T-Lymphocyte Subsets
  • Peptide Fragments
  • Myelin-Oligodendrocyte Glycoprotein
  • Multiple Sclerosis
  • Mice, Knockout
  • Mice
  • Lymphocyte Count
  • Immunophenotyping
  • Immunology
  • Immune Tolerance