Erythropoietin enhances endogenous haem oxygenase-1 and represses immune responses to ameliorate experimental autoimmune encephalomyelitis.

Both erythropoietin (EPO) and haem oxygenase-1 (HO-1), an anti-oxidative stress protein, have proven protective roles in experimental autoimmune encephalomyelitis (EAE), a reliable animal model of multiple sclerosis. In this study, EPO delivered intraperitoneally could reduce disease severity in myelin oligodendrocyte glycoprotein (MOG)–EAE mice. To assess the effect of EPO on endogenous HO-1 in EAE, we investigated expression of HO-1 mRNA by real-time polymerase chain reaction (RT–PCR), protein expression centrally and peripherally by Western blot and immunohistochemistry and mean fluorescence intensity of splenic HO-1 by flow cytometry.

Decoy receptor 3 ameliorates experimental autoimmune encephalomyelitis by directly counteracting local inflammation and downregulating Th17 cells.

To investigate the therapeutic potential of decoy receptor 3 (DcR3) in multiple sclerosis (MS), we used intrathecal (IT) administration of DcR3 into C57/BL6 mice with experimental autoimmune encephalomyelitis (EAE). DcR3 significantly ameliorated EAE symptoms as shown by a lower clinical score and less inflammation in the spinal cord. The expression of TNF-alpha, IFN-gamma, and IL-17 was lower in the spinal cord in IT DcR3-treated mice.