Study Of A Novel Recombinant Immunotoxin MMIP-1α-DT390 To Treat Mouse Experimental Autoimmune Encephalomyelitis

Objective There are no specific treatments for autoimmune disease in human currently, and multiple sclerosis(MS) is no exception. Experimental autoimmune encephalomyelitis(EAE) is T cell mediated demyelinating disease of the central nervous system(CNS) and serves as a well-established animal model for MS. The widely accepted pathogenetic process of EAE and MS is that activated T cells migrate to the CNS and develop inflammatory lesion, and some chemokines and their receptors preferentially expressed in T cells are involved in the pathogenesis. EAE can be induced by Myelin Basic Protein(MBP), Proteolipid Protein(PLP), Myelin Oligodendrocyte Glycoprotein(MOG) or Myelin Associated Glycoprotein(MAG), et al. In the study we prefered MBP to inducing mouse EAE model. It has been confirmed that many chemokine receptors are expressed in the membranes of activated T cells. CCR5 is over-expressed in the activated T cells membrane and might be an ideal target for the immunotherapy. In the study we choose MIP-1α, one of the ligand of CCR5, as the target moiety.