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- Title
Galectin-1 is essential for the induction of MOG<sub>35-55</sub>-based intravenous tolerance in experimental autoimmune encephalomyelitis.
- Authors
Mari, Elisabeth R.; Rasouli, Javad; Ciric, Bogoljub; Moore, Jason N.; Conejo‐Garcia, José R.; Rajasagi, Naveen; Zhang, Guang‐Xian; Rabinovich, Gabriel A.; Rostami, Abdolmohamad
- Abstract
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.
- Publication
European Journal of Immunology, 2016, Vol 46, Issue 7, p1783
- ISSN
0014-2980
- Publication type
Article
- DOI
10.1002/eji.201546212