MECHANISMS FOR THE INHIBITION OF DEVELOPMENT IN ENCEPHALOMYELITIS IN MICE LACKING THE EXPRESSION OF A CHEMOKINE REQUIRED FOR T CELL MIGRATION.

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We have found a mutant mouse strain with DDD background, plt (paucity of lymph node T cells) mouse, in which T cells are unable to migrate into the T cell areas in lymph nodes, Peyer's patches, or spleen white pulp. Antigen-stimulated dendritic cells do not entry into the T cell zones either. These mice lack the expression of secondary lymphoid tissue chemokine (SLC)s, which results from the deletion of SLC gene.We examined the development of experimental allergic encephalomyelitis (EAE) in these mutant mice. When these mice were immunized with myelin basic protein (MBP), EAE developed with a fewer frequency than in the control mice. Even when the MBP-immunized mutant mice developed EAE, the clinical score in these mice was much lower than in the control mice. For further analysis, we established C57BL/6 mice with the deletion of SLC gene, and immunized with MOG35-55 peptide. C57BL/6-plt mice were also resistant to the development of EAE. MBP- or MOG-specific T cells play a critical role to develop EAE. It might be possible that these T cells were not induced in plt mice immunized with MBP or MOG. However, this possibility seems unlikely, since in vivo T cell-priming with a protein antigen was not affected in these mice. These findings suggest that a chemokine is able to control the EAE development. Our findings also raised a possibility that a chemokine might be able to control multiple sclerosis.