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Neutralization of the Chemokine CXCL10 Reduces Inflammatory Cell Invasion and Demyelination and Improves Neurological Function in a Viral Model of Multiple Sclerosis

Michael T. Liu, Hans S. Keirstead and Thomas E. Lane
J Immunol October 1, 2001, 167 (7) 4091-4097; DOI: https://doi.org/10.4049/jimmunol.167.7.4091
Michael T. Liu
*Molecular Biology and Biochemistry and
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Hans S. Keirstead
†Anatomy and Neurobiology, and
‡Reeve-Irvine Research Center, University of California, Irvine, CA 92612
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Thomas E. Lane
*Molecular Biology and Biochemistry and
†Anatomy and Neurobiology, and
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Abstract

Intracerebral infection of mice with mouse hepatitis virus (MHV) results in an acute encephalomyelitis followed by a chronic demyelinating disease with clinical and histological similarities with the human demyelinating disease multiple sclerosis (MS). Following MHV infection, chemokines including CXC chemokine ligand (CXCL)10 (IFN inducible protein 10 kDa), CXCL9 (monokine induced by IFN-γ), and CC chemokine ligand 5 (RANTES) are expressed during both acute and chronic stages of disease suggesting a role for these molecules in disease exacerbation. Previous studies have shown that during the acute phase of infection, T lymphocytes are recruited into the CNS by the chemokines CXCL10 and CXCL9. In the present study, MHV-infected mice with established demyelination were treated with antisera against these two chemokines, and disease severity was assessed. Treatment with anti-CXCL10 reduced CD4+ T lymphocyte and macrophage invasion, diminished expression of IFN-γ and CC chemokine ligand 5, inhibited progression of demyelination, and increased remyelination. Anti-CXCL10 treatment also resulted in an impediment of clinical disease progression that was characterized by a dramatic improvement in neurological function. Treatment with antisera against CXCL9 was without effect, demonstrating a critical role for CXCL10 in inflammatory demyelination in this model. These findings document a novel therapeutic strategy using Ab-mediated neutralization of a key chemokine as a possible treatment for chronic human inflammatory demyelinating diseases such as MS.

  • Received March 13, 2001.
  • Accepted July 30, 2001.
  • Copyright © 2001 by The American Association of Immunologists
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The Journal of Immunology: 167 (7)
The Journal of Immunology
Vol. 167, Issue 7
1 Oct 2001
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Neutralization of the Chemokine CXCL10 Reduces Inflammatory Cell Invasion and Demyelination and Improves Neurological Function in a Viral Model of Multiple Sclerosis
Michael T. Liu, Hans S. Keirstead, Thomas E. Lane
The Journal of Immunology October 1, 2001, 167 (7) 4091-4097; DOI: 10.4049/jimmunol.167.7.4091

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Neutralization of the Chemokine CXCL10 Reduces Inflammatory Cell Invasion and Demyelination and Improves Neurological Function in a Viral Model of Multiple Sclerosis
Michael T. Liu, Hans S. Keirstead, Thomas E. Lane
The Journal of Immunology October 1, 2001, 167 (7) 4091-4097; DOI: 10.4049/jimmunol.167.7.4091
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