The Study On Foxp3 Expression In Brains And Spleens In Chronic Sustained Model Of Experimental Autoimmune Encephalomyelitis

Objective To investigate the changes of Foxp3mRNA expression in brains and spleens of induced chronic non-remitting model of experimental autoimmune encephalomyelitis (EAE), and discuss the mechanism of Foxp3 on EAE/MS.Methods 72 adult female C57BL/6 mice were randomly divided into the adjuvant -control group,EAE group, TGF-131 treatment group and adjuvant treatment-control group. MOG35-55 and CFA were injected into subcutaneous in EAE groups. Animals in TGF-β1 treatment groups received TGF-β1 subcutaneous injection, in addition to immunization. PBS was injected subcutaneously in adjuvant treatment-control group as treatment-control.At the onset, peak and chronic post-immunization,the group mice were sacrificed.The expression of Foxp3mRNA in brains and spleens were detected by RT-PCR.Results 83.3% mices in EAE group were developed a progressive paralysis, which peaked at 20-24 days, and then exhibited a chronic disease with a partial clinical recovery.In contrast, 88.9 % mices in TGF-β1 treatment group developed the ealier progressive paralysis, which peaked at 17-22 days,and were more prone to recovery. There were no remarkable difference between the adjuvant treatment-control group and the EAE group. The expression of Foxp3 mRNA of brains or spleens in the EAE group or the adjuvant treatment-control group decreased at early, followed by a descent in the peak phase and increased in the chronic phase(p＜0.05). While in TGF-β1 treatment groups, The expression of Foxp3 mRNA dramatically deceased (p＜0.05) in the peak phase and increased dramaticly in the chronic phase(p＜0.05) in contrast to the EAE group or the adjuvant treatment-control group.The expression of Foxp3 mRNA in the brains increased copared to the spleens no matter in the EAE group or the TGF-β1/adjuvant treatment group(p＜0.05).Conclusion1. The expression of Foxp3 was correlated with the severity and the course of disease.2.The effect of exogenous TGF-β1 on the EAE model is complicated. Mices in TGF-β1 treatment group developed more progressive symptoms and were more prone to recover than those in the EAE group and adjuvant treatment-control group.