Abstract
During the past decade, a great deal of information has contributed to our understanding of the immunosuppressive pathways that operate during the resolution of autoimmune pathology, including central nervous system (CNS) inflammation. Activation of these pathways is accomplished through the integration of an intricate network of inhibitory signals and immune suppressive cells, including regulatory T cells, myeloid-derived suppressor cells, 'alternatively activated' macrophages and tolerogenic dendritic cells (DCs). During the course of inflammatory diseases, immature or mature DCs may be licensed by different stimuli (e.g. cytokines, neuropeptides and growth factors) to become tolerogenic and suppress pathogenic T cell responses, thus emphasizing the outstanding plasticity of these cells. Recent findings have shed light to an immunoregulatory circuit by which galectin-1, an endogenous glycan-binding protein, favors the differentiation of regulatory DCs which promote T cell tolerance and contribute to resolution of autoimmune pathology through mechanisms involving IL-27 and IL-10. Together with the ability of galectin-1-glycan interactions to selectively blunt T helper (Th)1 and Th17 responses, this effect provides a rational e...Continue Reading
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