Mechanism of MOG i. p. for protecting mice from EAE

Objective To investigate mechanisms underlying the prevention of experimental autoimmune encephalomyelitis (EAE) in mice by intraperitoneal infusion of myelin oligodendrocyte glycoprotein 35-55 (MOG35-55) (MOG i. p.). Methods C57BL/6 mice were immunized with MOG35-55 to establish the model of EAE and then were intraperitoneally injected daily with MOG35-55 or ovalbumin (OVA, served as control) from day 6 to day 16. EAE was evaluated daily using a general clinical scoring system and histological analysis. Numbers of lymphocytes in peripheral blood and central nervous system (CNS) were detected at different time points. Effects of MOG i. p. on the migration of MOG-T cells in vivo were analyzed by an adoptive transfer experiment. Maturation of splenic antigen-presenting cells (APCs) and migration of MOG-T cells in vitro were examined by fluorescence activated cell sorting (FACS) and a Transwell system, respectively. Results MOG i. p. protected the mice from development of EAE by blocking the lymphocyte recruitment to CNS. More effector T cells were trapped in the periphery of EAE and naive mice in adoptive transfer experiment after MOG i. p. treatment. MOG i. p. induced the maturation of splenic APCs and enhanced the expression of CD80, CD86 and major histocompatibility complex class Ⅱ (MHCⅡ) molecules. Mature APCs blocked the recruitment of effector T cells to CNS. Conclusion MOG i. p. protects mice from EAE by inducing the maturation of splenic APCs. Key words: Experimental autoimmune encephalomyelitis; Immune tolerance; Antigen-presenting cell; Cell migration