Abstract: Experimental autoimmune encephalomyelitis (EAE) is a Th1-mediated autoimmune disease of the central nervous system that is widely used as an animal model of multiple sclerosis (MS). In this study it was demonstrate that CXCL13, a chemokine involved in the development of secondary lymphoid tissues, is expressed in CD11c+ myeloid cells that accumulate in EAE lesions. Blockade or deficiency of CXCL13 ameliorates clinical EAE, both during acute and relapsing stages. CXCL13 deficiency did not inhibit the priming or differentiation of autoimmune effector T-cells in the periphery, but appeared to exert its effects during the effector phase of pathogenesis. These findings indicate that reagents that antagonize or inhibit CXCL13 are useful for the treatment of neuroinflammatory diseases such as MS.

Abstract: Experimental autoimmune encephalomyelitis (EAE) is a Th1-mediated autoimmune disease of the central nervous system that is widely used as an animal model of multiple sclerosis (MS). In this study it was demonstrate that CXCL13, a chemokine involved in the development of secondary lymphoid tissues, is expressed in CD11c+ myeloid cells that accumulate in EAE lesions. Blockade or deficiency of CXCL13 ameliorates clinical EAE, both during acute and relapsing stages. CXCL13 deficiency did not inhibit the priming or differentiation of autoimmune effector T-cells in the periphery, but appeared to exert its effects during the effector phase of pathogenesis. These findings indicate that reagents that antagonize or inhibit CXCL13 are useful for the treatment of neuroinflammatory diseases such as MS.

Abstract: Experimental autoimmune encephalomyelitis (EAE) is a Th1-mediated autoimmune disease of the central nervous system that is widely used as an animal model of multiple sclerosis (MS). In this study it was demonstrate that CXCL13, a chemokine involved in the development of secondary lymphoid tissues, is expressed in CD11c+ myeloid cells that accumulate in EAE lesions. Blockade or deficiency of CXCL13 ameliorates clinical EAE, both during acute and relapsing stages. CXCL13 deficiency did not inhibit the priming or differentiation of autoimmune effector T-cells in the periphery, but appeared to exert its effects during the effector phase of pathogenesis. These findings indicate that reagents that antagonize or inhibit CXCL13 are useful for the treatment of neuroinflammatory diseases such as MS.

Abstract: Experimental autoimmune encephalomyelitis (EAE) is a Th1-mediated autoimmune disease of the central nervous system that is widely used as an animal model of multiple sclerosis (MS). In this study it was demonstrate that CXCL13, a chemokine involved in the development of secondary lymphoid tissues, is expressed in CD11c+ myeloid cells that accumulate in EAE lesions. Blockade or deficiency of CXCL13 ameliorates clinical EAE, both during acute and relapsing stages. CXCL13 deficiency did not inhibit the priming or differentiation of autoimmune effector T-cells in the periphery, but appeared to exert its effects during the effector phase of pathogenesis. These findings indicate that reagents that antagonize or inhibit CXCL13 are useful for the treatment of neuroinflammatory diseases such as MS.