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The change of PD1, PDL1 in experimental autoimmune encephalomyelitis treated by 1,25(OH)2D3.

J Neuroimmunol. 2020; 
Cao Q1, Zheng C1, Xie Z2, Liu L1, Zhu J3, Jin T4.
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Custom DNA/RNA Oligos For the induction of EAE, myelin oligodendrocyte glycoprotein 35–55 (MOG35–55) peptide (GenScript, Piscataway, NJ) emulsified with complete Freund's adjuvant (Sigma Aldrich, St Louis, MO) containing 8 mg/ml of heat-inactivated Mycobacterium tuberculosis (Difco, Detroit, MI) was given to the mice by hypodermic injection. Get A Quote

摘要

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).,Copyright © 2019... More

关键词

1,25-dihydroxyvitamin D(3); Experimental autoimmune encephalomyelitis; Multiple sclerosis; Programmed death 1; Programmed death ligand 1; Tolerogenic dendritic cells