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*
Department of Pathology, Harvard Medical School, Boston, MA 02115; and
Millennium Pharmaceuticals, Cambridge, MA 02139
Astrocytes are specialized cells of the CNS that are implicated in
the pathogenesis of multiple sclerosis and experimental allergic
encephalomyelitis. In acute and relapsing-remitting experimental
allergic encephalomyelitis, the neutrophil chemoattractant CXC
chemokines macrophage-inflammatory protein (MIP)-2 and KC are
associated with reactive astrocytes in the parenchyma. In vitro
treatment of primary astrocyte cultures with nanomolar concentrations
of MIP-2 or KC markedly up-regulated expression of the monocyte/T cell
chemoattractants monocyte chemoattractant protein-1, inflammatory
protein-10, and RANTES by a mechanism that includes stabilization of
mRNA. Production of TNF-
and IL-6 transcripts were also noted, as
was autocrine induction of MIP-2 and KC message. In addition, low
levels of MIP-1 and MIP-1ß were induced following treatment with
MIP-2 or KC. These effects are specific to astrocytes as MIP-2
treatment of microglial cells failed to elicit chemokine production.
The astrocyte chemokine receptor for MIP-2 has 2.5 nM affinity for
ligand. Astrocytes from CXCR2-deficient mice still respond to KC and
MIP-2, indicating the presence of an alternative or novel high affinity
receptor for these ligands. We propose that this KC/MIP-2 chemokine
cascade may contribute to the persistence of mononuclear cell
infiltration in demyelinating autoimmune
diseases.
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