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The Influence of the Proinflammatory Cytokine, Osteopontin, on Autoimmune Demyelinating Disease
Dorothée Chabas,1*Sergio E. Baranzini,2*Dennis Mitchell,1Claude C. A. Bernard,3Susan R. Rittling,4David T. Denhardt,4Raymond A. Sobel,5Christopher Lock,1Marcela Karpuj,12Rosetta Pedotti,1Renu Heller,6Jorge R. Oksenberg,2Lawrence Steinman1
Multiple sclerosis is a demyelinating disease, characterized
by inflammation in the brain and spinal cord, possibly due toautoimmunity. Large-scale sequencing of cDNA libraries, derivedfrom
plaques dissected from brains of patients with multiple sclerosis(MS),
indicated an abundance of transcripts for osteopontin (OPN).Microarray
analysis of spinal cords from rats paralyzed by experimentalautoimmune
encephalomyelitis (EAE), a model of MS, also revealedincreased OPN
transcripts. Osteopontin-deficient mice were resistantto progressive
EAE and had frequent remissions, and myelin-reactiveT cells in
OPN-/- mice produced more interleukin 10 and less
interferon- thanin OPN+/+ mice. Osteopontin thus
appears to regulate T helper cell-1
(TH1)-mediateddemyelinating disease, and it may
offer a potential target inblocking development of progressive MS.
1 Department of Neurology and Neurological
Sciences, Beckman Center for Molecular Medicine, B002, Stanford, CA
94305, USA.
2 Department of Neurology, University of
California at San Francisco School of Medicine, San Francisco, CA
94143, USA.
3 Neuroimmunology Laboratory, Department
of Biochemistry, La Trobe University, Bundoora, Victoria, 3083 Australia.
4 Department of Cell Biology and
Neuroscience, Rutgers University, Piscataway, NJ 08854, USA.
5 Department of Pathology (Neuropathology), Stanford
University School of Medicine, Stanford, CA 94305, USA.
6 Roche Bioscience, 3401 Hillview Avenue, Palo Alto,
CA 94304, USA.
*
These authors contributed equally to this work.
These senior authors contributed equally to this work.
To whom editorial correspondence should be addressed.
E-mail: steinman{at}stanford.edu
The editors suggest the following Related Resources on Science sites:
In Science Magazine
TECHNICAL COMMENTS
Thomas Blom, Ahnders Franzén, Dick Heinegård, and Rikard Holmdahl (21 March 2003) Science299 (5614), 1845a.
[DOI: 10.1126/science.1078985] |Full Text »|PDF »
TECHNICAL COMMENTS
Lawrence Steinman, Sawsan Youssef, Natalie Van Venrooij, Dorothée Chabas, Sergio E. Baranzini, Susan Rittling, David Denhardt, Raymond A. Sobel, Christopher Lock, Rosetta Pedotti, and Jorge R. Oksenberg (21 March 2003) Science299 (5614), 1845b.
[DOI: 10.1126/science.1080223] |Full Text »|PDF »
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Molecular pathophysiology in Tay-Sachs and Sandhoff diseases as revealed by gene expression profiling.
R. Myerowitz, D. Lawson, H. Mizukami, Y. Mi, C. J. Tifft, and R. L. Proia (2002)
Hum. Mol. Genet.
11, 1343-1351
|Abstract »|Full Text »|PDF »
Cutting Edge: Attenuated Experimental Autoimmune Encephalomyelitis in Eta-1/Osteopontin-Deficient Mice.
M. Jansson, V. Panoutsakopoulou, J. Baker, L. Klein, and H. Cantor (2002)
J. Immunol.
168, 2096-2099
|Abstract »|Full Text »|PDF »
Inflammatory Mediators in Uveitis: Differential Induction of Cytokines and Chemokines in Th1- Versus Th2-Mediated Ocular Inflammation.
E. F. Foxman, M. Zhang, S. D. Hurst, T. Muchamuel, D. Shen, E. F. Wawrousek, C.-C. Chan, and I. Gery (2002)
J. Immunol.
168, 2483-2492
|Abstract »|Full Text »|PDF »
Osteopontin: A Molecule Important in Multiple Sclerosis.
(2001)
Journal Watch (General)
2001, 5
|Full Text »
than in OPN+/+ mice. Osteopontin thus
appears to regulate T helper cell-1
(TH1)-mediated demyelinating disease, and it may
offer a potential target in blocking development of progressive MS.
