Mechanism of immune tolerance induced by soluble myelin oligodendrocyte glycoprotein in mice with experimental autoimmune encephalomyelitis

: Objective To explore the mechanism of immune tolerance induced by soluble MOG35-55 (MOG) peptide in mice with experimental autoimmune encephalomyelitis (EAE). Methods EAE mice were randomly divided into three groups, MOG, OVA and control groups, which were injected intraperitoneally with MOG, OVA peptide and PBS, respectively, from day 6 to day 16 after EAE induction. Lymphocytes in the spleen and CNS were enumerated and their phenotypes and function were analyzed by flow cytometry to explore the role of T cell migration in MOG-induced EAE tolerance. Next, CD11b+ antigen presenting cells (APCs) in the spleen and CNS infiltration were analyzed by flow cytometry to evaluate their maturation, and the role of mature APCs in blocking MOG-CD4+ T cells trafficking to CNS was determined by immunofluorescence technique. Results MOG trapped effector T cells in the spleen and protected mice from EAE. MOG triggered the maturation of splenic APCs, while prevented the maturation of CNS-infiltrating APCs. MOG-loaded APCs could interact with MOG reactive CD4+ T cells and limit their migration. Conclusion MOG can protect mice from EAE by inducing the maturation of splenic APCs that interact with MOG-T cells and trap them in the periphery.