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From the Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California
Chemokines may be important in the control of leukocytosis in
inflammatory disorders of the central nervous system. We studied
cerebral chemokine expression during the evolution of diverse
neuroinflammatory disorders in transgenic mice with astrocyte glial
fibrillary acidic protein-targeted expression of the cytokines
IL-3, IL-6, or IFN-
and in mice with experimental
autoimmune encephalomyelitis. Distinct chemokine gene expression
patterns were observed in the different central nervous system
inflammatory models that may determine the phenotype and perhaps the
functions of the leukocytes that traffic into the brain.
Notably, high expression of C10 and C10-related genes was found
in the cerebellum and spinal cord of GFAP-IL3 mice with inflammatory
demyelinating disease and in mice with experimental autoimmune
encephalomyelitis. In both these neuroinflammatory models, C10
RNA and protein expressing cells were predominantly
macrophage/microglia and foamy macrophages present within demyelinating
lesions as well as in perivascular infiltrates and meninges.
Intracerebroventricular injection of recombinant C10 protein promoted
the recruitment of large numbers of Mac-1+ cells
and, to a much lesser extent, CD4+
lymphocytes into the meninges, choroid plexus,
ventricles, and parenchyma of the brain. Thus, C10 is a
prominent chemokine expressed in the central nervous system in
experimental inflammatory demyelinating disease that, we
show, also acts as a potent chemotactic factor for the
migration of these leukocytes to the brain.
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