CXC Chemokine Ligand 13 Plays a Role in Experimental Autoimmune Encephalomyelitis

• Published in: Journal of Immunology 2006-06, Vol.176 (12), p.7676-7685
• Main Authors: Bagaeva, Ludmila V, Rao, Praveen, Powers, James M, Segal, Benjamin M
• Format: Article
• Language: English
• Subjects: Acute Disease; Amino Acid Sequence; Animals; Cell Movement - genetics; Cell Movement - immunology; Cells, Cultured; Chemokine CXCL13; Chemokines, CXC - biosynthesis; Chemokines, CXC - deficiency; Chemokines, CXC - genetics; Chemokines, CXC - physiology; Down-Regulation - genetics; Down-Regulation - immunology; Encephalomyelitis, Autoimmune, Experimental - genetics; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - pathology; Encephalomyelitis, Autoimmune, Experimental - prevention & control; Glycoproteins - administration & dosage; Glycoproteins - immunology; Immunity, Active; Leukocytes, Mononuclear - immunology; Leukocytes, Mononuclear - metabolism; Leukocytes, Mononuclear - pathology; Lymphocyte Activation - genetics; Lymphocyte Activation - immunology; Mice; Mice, Inbred C57BL; Mice, Transgenic; Molecular Sequence Data; Myelin-Oligodendrocyte Glycoprotein; Peptide Fragments - administration & dosage; Peptide Fragments - immunology; Receptors, Chemokine; Receptors, CXCR5; Receptors, Cytokine - biosynthesis; Recurrence; RNA, Messenger - biosynthesis; Spinal Cord - immunology; Spinal Cord - metabolism; Spinal Cord - pathology; T-Lymphocyte Subsets - immunology; T-Lymphocyte Subsets - metabolism
• ISSN: 0022-1767; 1550-6606; 1365-2567
• DOI: 10.4049/jimmunol.176.12.7676

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.