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CUTTING EDGE |



*
Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92612;
Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037; and
Department of Immunology, The Lerner Research Institute, Cleveland, OH 44195
The contribution of the T cell chemoattractant chemokine
IFN-inducible protein 10 (IP-10) in host defense following viral
infection of the CNS was examined. IP-10 is expressed by astrocytes
during acute encephalomyelitis in mouse hepatitis virus-infected mice,
and the majority of T lymphocytes infiltrating into the CNS expressed
the IP-10 receptor CXCR3. Treatment of mice with anti-IP-10
antisera led to increased mortality and delayed viral clearance from
the CNS as compared with control mice. Further, administration of
anti-IP-10 led to a >70% reduction (p
0.001) in CD4+ and CD8+ T lymphocyte
infiltration into the CNS, which correlated with decreased
(p
0.01) levels of IFN-
. These data indicate
that IP-10 functions as a sentinel molecule in host defense and is
essential in the development of a protective Th1 response against viral
infection of the CNS.
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