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- Ludmila V. Bagaeva
- *Department of Neurology,
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- Praveen Rao
- *Department of Neurology,
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- James M. Powers
- †Department of Pathology,
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- Benjamin M. Segal
- *Department of Neurology,
抄録
<jats:title>Abstract</jats:title><jats:p>Experimental autoimmune encephalomyelitis (EAE) is a Tcell-mediated autoimmune disease of the CNS that is widely used as an animal model of multiple sclerosis. In this study, we investigate the role of CXCL13, a chemokine involved in the development and organization of secondary lymphoid tissues, in the pathogenesis of EAE. We detected CXCL13 mRNA and protein in spinal cords of mice with EAE. CXCL13-deficient mice exhibited a mild, self-limited form of disease. CXCL13 appeared to be important for the establishment of chronic white matter lesions. Furthermore, adoptive transfer experiments with CXCL13-deficient hosts indicate that the chemokine plays a distinct role during the effector phase. Our findings raise the possibility that reagents that antagonize or inhibit CXCL13 might be useful for the treatment of neuroinflammatory diseases such as multiple sclerosis.</jats:p>
収録刊行物
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- The Journal of Immunology
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The Journal of Immunology 176 (12), 7676-7685, 2006-06-15
The American Association of Immunologists