Abstract
Experimental autoimmune encephalomyelitis (EAE) is a common animal model that has the same pathology and pathogenesis as multiple sclerosis (MS). Dendritic cells (DCs) exert an important role in central and peripheral tolerance. DCs not only drive T cell priming and differentiation via playing antigen presentation function but mediate the resolution of advancing immune responses with its tolerogenic effect. In this study, we employed 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) to induce tolerogenic dendritic cells (VD3-DCs) revealing their therapeutic effect through an increase in the development of the negative regulatory signaling pathway programmed death 1 (PD1)/programmed death ligand 1 (PDL1).
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