Role of galectins in inflammation and remyelination in multiple sclerosis

Multiple sclerosis is a chronic, heterogeneous disease caused by attacks on the myelin sheaths in brain white matter by autoimmune T-lymphocytes. No cure or effective treatment exists because it is not fully known what triggers the onset of the disease and why remyelination is often impaired. It is likely the result of a dysregulation of one or (more likely) multiple processes involved in the autoimmune inflammation-mediated demyelination and remyelination. Galectins are a group of beta-galactoside sugar-binding proteins known for their involvement in various extracellular and intracellular mechanisms, for example cell-matrix, matrix-matrix interactions, cell cycle regulation and pre-mRNA splicing. They are also known to modulate the immunesystem in various ways. This review analyzes the role galectins play in the various processes that are instrumental to inflammation mediated demyelination and remyelination in multiple sclerosis.