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CUTTING EDGE |
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Department of Pathology, Immunobiology Center, Robert H. Lurie Cancer Center, and Institute for Neuroscience, Northwestern University Medical School, Chicago, IL 60611; and
Department of Neurosciences, Lerner Research Institute and Mellen Center for Multiple Sclerosis Treatment and Research, Cleveland Clinic Foundation, Cleveland, OH 44195
Experimental autoimmune encephalomyelitis (EAE) is a CD4+ Th1-mediated 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, chemokines are highly expressed in the central nervous system with a tight temporal relationship to disease activity. Second, in vivo neutralization studies showed a distinct role for specific chemokines in the evolution of the process. Third, the selective and differential expression of chemokines in differing models of EAE bears a close relationship to the patterns of inflammatory pathology. Fourth, the spatial distribution of chemokine expression could plausibly contribute to lesion architecture. Finally, preliminary observations in MS material suggest that chemokine expression observed in EAE may provide useful information regarding the pathogenesis of inflammation in MS. We propose that temporal and spatial expression of chemokines are crucial factors, complementing adhesion molecule up-regulation, that regulate EAE disease activity.
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T. E. Lane, M. T. Liu, B. P. Chen, V. C. Asensio, R. M. Samawi, A. D. Paoletti, I. L. Campbell, S. L. Kunkel, H. S. Fox, and M. J. Buchmeier A Central Role for CD4+ T Cells and RANTES in Virus-Induced Central Nervous System Inflammation and Demyelination J. Virol., February 1, 2000; 74(3): 1415 - 1424. [Abstract] [Full Text]
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C. Teuscher, R. J. Butterfield, R. Z. Ma, J. F. Zachary, R. W. Doerge, and E. P. Blankenhorn Sequence Polymorphisms in the Chemokines Scya1 (TCA-3), Scya2 (Monocyte Chemoattractant Protein (MCP)-1), and Scya12 (MCP-5) Are Candidates for eae7, a Locus Controlling Susceptibility to Monophasic Remitting/Nonrelapsing Experimental Allergic Encephalomyelitis J. Immunol., August 15, 1999; 163(4): 2262 - 2266. [Abstract] [Full Text] [PDF]
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J. M. Soos, T. A. Ashley, J. Morrow, J. C. Patarroyo, B. E. Szente, and S. S. Zamvil Differential expression of B7 co-stimulatory molecules by astrocytes correlates with T cell activation and cytokine production Int. Immunol., July 1, 1999; 11(7): 1169 - 1179. [Abstract] [Full Text] [PDF]
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 K. E. Balashov, J. B. Rottman, H. L. Weiner, and W. W. Hancock CCR5+ and CXCR3+ T cells are increased in multiple sclerosis and their ligands MIP-1alpha and IP-10 are expressed in demyelinating brain lesions PNAS, June 8, 1999; 96(12): 6873 - 6878. [Abstract] [Full Text] [PDF]
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