Investigate the DNA methylation pattern of T cell cytokines and Programmed cell death-ligand 1 on Antigen presenting cell in experimental autoimmune encephalomyelitis Advisor: SHU-FEN WU Date: 2015/10/02 Student: YONG-LIN CHANG Abstract Multiple sclerosis (MS) is a Th1/Th17 CD4+ T cell-mediated chronic autoimmune disease of the central nervous system. Relapsing-remitting MS (RRMS) have accounted for the most of the MS. Experimental autoimmune encephalomyelitis (EAE) is the most commonly animal model using to study of the MS. In EAE model, immunized with the mixture of mycobacterium and myelin antigen will activate dendritic cell (DC) to present myelin antigen for T cell activation. T cells expand and release inflammatory mediators and cytokines such as IFN-r and IL-17. In recent study, distant T helper lineage has been shown to involve epigenetic regulation of the differentiation and polarization. The epigenetic pattern has not been detailed study in EAE model and MS. Therefore, we aimed to identify the DNA methylation pattern and disease changes in EAE model .In this study, we induced EAE and observed the score. It showed that disease progression was correlated with expression of IFN-r. Then we used pyrosequencing to detect region of IFN-r methylation pattern. We found that the regions of intron and CNS-6 of IFN-r was hypo-methylation in EAE mice, while healthy mice were hyper-methylation. On the other hand, antigen presenting cell played an important role in immune response. In EAE model, disease progression was regulated by programmed cell death-ligand 1(PDL1).In primary data of DC, the DNA methylation level of 5-aza-(DNMT inhibitor) or DMSO- treated JAWSâ…ˇ(mice DC cell line) had no difference at PDL1 by pyrosequencing. In the future, we will compare PDL1 knockout mice to wild type mice in EAE progression and DNA methylation of different regions of IFN-r and IL-17.