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-Inducible Protein-10) Control of Encephalitogenic CD4+ T Cell Accumulation in the Central Nervous System During Experimental Autoimmune Encephalomyelitis1
*
Department of Pathology, Immunobiology Center, Robert H. Lurie Cancer Center, and Institute for Neuroscience, Northwestern University Medical School, Chicago, IL 60611;
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109; and
Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Charlestown, MA 02129
Experimental autoimmune encephalomyelitis (EAE) is a
CD4+ Th1-mediated demyelinating disease of the CNS that
serves as a model for multiple sclerosis. A critical event in the
pathogenesis of EAE is the entry of both Ag-specific and Ag-nonspecific
T lymphocytes into the CNS. In the present report, we investigated the
role of the CXC chemokine CXCL10 (IFN-
-inducible protein-10) in the
pathogenesis of EAE. Production of CXCL10 in the CNS correlated with
the development of clinical disease. Administration of anti-CXCL10
decreased clinical and histological disease incidence, severity, as
well as infiltration of mononuclear cells into the CNS. Anti-CXCL10
specifically decreased the accumulation of encephalitogenic
PLP139–151 Ag-specific CD4+ T cells in the CNS
compared with control-treated animals. Anti-CXCL10 administration did
not affect the activation of encephalitogenic T cells as measured by
Ag-specific proliferation and the ability to adoptively transfer EAE.
These results demonstrate an important role for the CXC chemokine
CXCL10 in the recruitment and accumulation of inflammatory mononuclear
cells during the pathogenesis of EAE.
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