J Neuroimmunol 2003 Apr;137(1-2):109-16
Bagaeva LV, Williams LP, Segal BM.
Department of Neurology, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Box 605, 14642, Rochester, NY, USA
Experimental autoimmune encephalomyelitis (EAE) is an inflammatory demyelinating disease with similarities to multiple sclerosis (MS).
It is induced in mice by the transfer of myelin-reactive T cells.
Here we demonstrate that IL-12 stimulates myelin-reactive T cells to up-regulate the beta-chemokine receptor, CCR5, in correlation with the acquisition of central nervous system-infiltrating and encephalitogenic properties.
These effects of IL-12 are IFNgamma-independent.
The CCR5 ligands, RANTES and MIP-1alpha, are expressed in the spinal cords of mice at EAE onset.
Our results suggest that reagents that block CCR5/beta-chemokine interactions and/or antagonize IL-12 might be useful for treatment of autoimmune demyelination.