Novel Treatments for Autoimmune Neuroinflammatory Diseases including Multiple Sclerosis
Posted Jun 15 2010 5:00pm
Description of Invention: Multiple sclerosis is caused when T cells mistakenly attack myelin, the protective fatty layer surrounding neurons in the brain and spinal cord, to initiate autoimmune responses and inflammation of the central nervous system (CNS). An increase in T cell-endothelial cell interactions and/or increased infiltration of immune cells to the CNS may play a role in the onset and/or progression of this disease.
Researchers at the NIH previously reported that extracellular adherence protein (Eap) produced by Staphylococcus aureus interacts with intercellular adhesion molecule 1 to prevent beta2-integrin-dependent inflammatory cell recruitment. They have now shown that Eap administration to mice with experimental autoimmune encephalomyelitis, a condition thought to be a model for human multiple sclerosis, blocks T cell recruitment to the brains of the EAE affected mice, inhibits the onset of this disease, and reverses paralysis. Eap also reduces delayed-type hypersensitivity in affected mice by inhibiting T cell infiltration and plasma leakage.
Available for licensing are methods for administering an Eap agent in an amount that will treat or prevent autoimmune neuroinflammatory diseases such as multiple sclerosis, decrease the infiltration of immune cells to the central nervous system, and inhibit T cell-endothelial cell interactions.
Potential non-toxic treatment for autoimmune neuroinflammatory diseases, such as multiple sclerosis
Potential therapy for alleviating symptoms associated with multiple sclerosis such as paralysis
Development Status: Animal data is available.
Inventors: Triantafyllos Chavakis (NCI)
Patent Status: HHS, Reference No. E-295-2005/0
T Chavakis et al. Staphylococcus aureus extracellular adherence protein serves as anti-inflammatory by inhibiting the recruitment of host leukocytes. Nat Med. 2002 Jul;8(7):687-693. [ PubMed abs ]
C Xie et al. Suppression of experimental autoimmune encephalomyelitis by extracellular adherence protein of Staphylococcus aureus. J Exp Med. 2006 Apr 17;203(4):985-994 . [ PubMed abs ]
Licensing Status: Available for exclusive and non-exclusive licensing.
Collaborative Research Opportunity: The National Cancer Institute Experimental Immunology Branch is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize Novel Treatments for Autoimmune Neuroinflammatory Diseases including Multiple Sclerosis. Please contact John Hewes, Ph.D., at 240-482-3453 for more information.
Portfolios: Central Nervous System Central Nervous System - Therapeutics In-vivo Data
For Additional Information Please Contact: Norbert Pontzer Ph.D., J.D. NIH Office of Technology Transfer 6011 Executive Blvd. Suite 325
Room 23, Rockville, MD 20852 United States Email: firstname.lastname@example.org Phone: 301-435-5502 Fax: 301-402-0220