CUTTING EDGE COMMENTARY - CHEMOKINE REGULATION OF EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS - TEMPORAL AND SPATIAL EXPRESSION PATTERNS GOVERN DISEASE PATHOGENESIS

Experimental autoimmune encephalomyelitis (EAE) is a CD4(+) Th1-mediat ed demyelinating disease of the central nervous system that serves as a model for multiple sclerosis (MS). There are several considerations that suggest a role for chemokines in the disease process. First, chem okines are highly expressed in the central nervous system with a tight temporal relationship to disease activity. Second, in vivo neutraliza tion studies showed a distinct role for specific chemokines in the evo lution of the process. Third, the selective and differential expressio n of chemokines in differing models of EAE bears a close relationship to the patterns of inflammatory pathology. Fourth, the spatial distrib ution of chemokine expression could plausibly contribute to lesion arc hitecture. Finally, preliminary observations in MS material suggest th at chemokine expression observed in EAE may provide useful information regarding the pathogenesis of inflammation in MS. We propose that tem poral and spatial expression of chemokines are crucial factors, comple menting adhesion molecule up-regulation, that regulate EAE disease act ivity.