Immunoneutralization of chemokines for the prevention and treatment of central nervous system autoimmune disease

William J. Karpus, Brian T. Fife, Kevin J. Kennedy

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


Chemokine-induced lymphocyte migration has long been hypothesized to regulate the appearance and continued presence of lymphocytes and monocytes in tissue-specific autoimmune diseases, including central nervous system autoimmune diseases such as multiple sclerosis. For instance, a large body of evidence points to the temporal association of chemokine expression with the appearance of T lymphocytes and monocytes/macrophages. Furthermore, experiments using mice with targeted mutations for chemokines have shown the importance of those molecules in the development of central nervous system autoimmune disease. We have hypothesized that temporal and spatial expression of chemokines is a key factor in the pathogenesis of experimental autoimmune encephalomyelitis and multiple sclerosis. To test our hypothesis we have employed the strategy of eliminating chemokine function by the passive transfer of chemokine-specific polyclonal antibodies. This approach has allowed us not only to test the function of chemokines in experimental autoimmune encephalomyelitis development, but also to ask questions about the roles of chemokines during disease progression. Moreover, this approach has allowed us to assess the efficacy of targeting chemokines and their receptors for treatment of ongoing disease. In the present report we summarize our experience using anti-chemokine administration for the prevention and treatment of experimental autoimmune encephalomyelitis as well as provide specific examples of how this approach is efficacious for disease treatment.

Original languageEnglish (US)
Pages (from-to)362-368
Number of pages7
Issue number4
StatePublished - Apr 1 2003
Externally publishedYes

Bibliographical note

Funding Information:
The authors thank Drs. Nicholas W. Lukacs (University of Michigan Medical School), Steven L. Kunkel (University of Michigan Medical School), and Robert M. Strieter (UCLA School of Medicine) for anti-chemokine reagents and valuable scientific discussions. This work was supported by PHS Grant NIH R01 NS34510.


  • Autoimmune encephalomyelitis
  • Central nervous system
  • Chemokines
  • EAE
  • Multiple sclerosis


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