Inhibition of experimental autoimmune encephalomyelitis by a novel small molecular weight proinflammatory cytokine suppressing drug

William J. Karpus*, Nathaneal Reynolds, Heather A. Behanna, Linda J. Van Eldik, D Martin Watterson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)73-78
Number of pages6
JournalJournal of Neuroimmunology
Volume203
Issue number1
DOIs
StatePublished - Oct 15 2008

Keywords

  • Chemokines, Minozac
  • Experimental autoimmune encephalomyelitis
  • Multiple sclerosis
  • Neuroinflammation
  • Proinflammatory cytokines
  • Pyridazine

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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