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  • Title: In vivo administration of plasmid DNA encoding recombinant immunotoxin DT390-IP-10 attenuates experimental autoimmune encephalomyelitis.
    Author: Chen W, Li H, Jia Y, Lv M, Li M, Feng P, Hu H, Zhang L.
    Journal: J Autoimmun; 2007 Feb; 28(1):30-40. PubMed ID: 17267177.
    Abstract:
    Experimental autoimmune encephalomyelitis (EAE) is a T-cell-mediated autoimmune demyelinating disease. The expression of chemokine receptor CXCR3 on activated T cells is crucial to direct the migration of effector cells into the inflammatory sites and initiate EAE. In this study we tested the effect of a novel recombinant immunotoxin targeting CXCR3(+) cells for EAE prevention. The immunotoxin construct DT390-IP-10-SRalpha consisted of interferon gamma-inducible protein 10 (IP-10), a ligand of CXCR3, as the targeting moiety, and a truncated diphtheria toxin (DT390) as the toxic moiety. In vitro transfection of DT390-IP-10-SRalpha into NIH3T3 cells resulted in expression of DT390-IP-10 which proved highly toxic to activated T cells. To evaluate the effect of DT390-IP-10-SRalpha on EAE prevention in vivo, cationic liposome-embedded DT390-IP-10-SRalpha was injected into the muscle of hind limbs of C57BL/6 mice immunized by myelin basic protein (MBP). DT390-IP-10-SRalpha-treated mice showed a delayed onset of EAE and milder symptoms compared to the mice treated with empty control plasmid or PBS alone. Immunohistochemical staining detected significantly reduced infiltrating CXCR3(+) cells in the inflammatory lesions of CNS from immunotoxin treated mice as compared to the controls. This study suggests that targeting CXCR3(+) T cells with recombinant immunotoxin could be achieved in vivo to delay and ameliorate murine EAE.
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