CXC chemokine ligand 13 plays a role in experimental autoimmune encephalomyelitis

被引:92
作者
Bagaeva, Ludmila V.
Rao, Praveen
Powers, James M.
Segal, Benjamin M.
机构
[1] Univ Rochester, Sch Med & Dent, Dept Neurol, Rochester, NY 14642 USA
[2] Univ Rochester, Sch Med & Dent, Dept Pathol, Rochester, NY 14642 USA
[3] Univ Rochester, Sch Med & Dent, Dept Microbiol & Immunol, Rochester, NY 14642 USA
[4] Univ Rochester, Sch Med & Dent, Ctr Canc, Rochester, NY 14642 USA
关键词
D O I
10.4049/jimmunol.176.12.7676
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:7676 / 7685
页数:10
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