Alleviation of experimental autoimmune encephalomyelitis by transferring low RelB expression tolerogenic dendritic cells

Abstract

AimsExperimental autoimmune encephalomyelitis (EAE) is a widely used mouse model of multiple sclerosis. Rather than inducing immune response, tolerogenic dendritic cells (tDCs) have the ability to induce immune tolerance. In previous studies, we induced tDCs by 1,25-(OH)2D3 and 1,25-(OH)2D3 DCs significantly alleviated EAE symptoms. As downstream targets of 1,25-(OH)2D3, inhibition of RelB and MyD88 expression in DCs might induce tDCs and has therapeutic effect of MS. MethodsKnockdown the expression of RelB and MyD88 with shRNA lentivirus to induce tDCs, adoptive transfer these tDCs to EAE mice, and investigate their therapeutic effects. ResultsReduction of RelB expression induced tDCs. After transferring into EAE mice, tDCs with low RelB expression significantly alleviate their symptoms as well as reduce the immune cell infiltration and demyelination in spinal cord. ConclusionRelB plays a key role in the antigen presenting function of DCs, and tDCs with low RelB expression is a potential treatment for EAE and MS.