| ObjectiveMultiple sclerosis (MS) is one of the familiar refractory autoimmune diseases characterized by demyelination in CNS, and can not be treated easily. The major remedial methods to MS which had been used were large doses of methyl- prednisolone, stem cell transplantation, the inhibitors of key enzymes such as cytosolic phospholipase A2 (cPLA2), plasma replacement, altered peptide ligands (APLs), T cell vaccination (TCV), and etc. ACTH, IFN-β1a (Avonex), IFN-β1b (Betaseron), Glatiramer acetate (Copaxone), Mitoxantrone, Natalizu mAb had been authorized by FDA to treat EAE in recently. Experimental autoimmune encephalomyelitis (EAE) or Experimental Allergic Encephalomyelitis (EAE) can be induced by Myelin Basic Protein (MBP) , Proteolipid Protein (PLP) , Myelin Oligodendrocyte Glycoprotein (MOG) or Myelin Associated Glycoprotein (MAG) , and etc. EAE has the similarclinical symptom, pathological changes in CNS, biochemical index compared with MS that has been widely used as a model of the acute/relapsing stage of multiple sclerosis.Immunotoxin is a hybrid molecule that consisting of a targeting moiety and a toxic moiety. Diphtheria toxin (DT) is an exotoxin secreted by diphtheria bacillus which has 535 amino acids. It is consisted of three domains which are catalytic domain, transmembrane domain and receptor binding domain. Truncated diphtheria toxin is often used as a toxic moiety because of its highly toxic to eukaryotic cells. Monoclonal antibodies as well as cytokines and chemokines are used as targeting moiety in construction of recombinant immunotoxins because of their specificities and high binding affinities to the target cells. Recombinant immunotoxins have been used to treat the malignant tumors, but few in the autoimmune disease.
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