Experimental autoimmune encephalomyelitis (EAE) is a T cell-mediated, autoimmune disease of the central nervous system (CNS) that serves as a model for various cellular and molecular aspects of the human disease, multiple sclerosis (MS). Although EAE has long been considered a T cell-mediated disease, macrophages play a role in disease pathogenesis and are known to accumulate in the CNS under the control of chemokines. In the present report we demonstrate that mice induced to develop EAE were treated with a small molecular weight molecule that suppresses proinflammatory cytokine production which resulted in significantly decreased clinical EAE, CNS CCL2 expression and CNS macrophage accumulation. These results demonstrate the efficacy of a novel class of therapeutic molecules for CNS demyelinating disease.
|Number of pages||6|
|Journal||Journal of Neuroimmunology|
|State||Published - Oct 15 2008|
Bibliographical noteFunding Information:
This work was supported by NS34510, AG028561, NS047586, and AG000260.
- Chemokines, Minozac
- Experimental autoimmune encephalomyelitis
- Multiple sclerosis
- Proinflammatory cytokines
ASJC Scopus subject areas
- Immunology and Allergy
- Clinical Neurology