Abstract

We shall investigate the mechanism by which a reduced carboxamidomethylated curarimetic neurotoxin of cobra venom origin protects guinea pigs against the development of experimental allergic encephalomyelitis (EAD), an animal model disease for human multiple sclerosis. Enzymatic cleavage of derivatized neurotoxin and chemical synthesis of specific toxin peptide fragments and analogs will be performed. These peptides will be used to test the idea that specific portions of the molecule control its immunosuppressive behavior. Immune cells derived from toxin or peptide protected animals will be transferred to histocompatible recipients; challenge with myelin basic protein will not induce EAE if unresponsiveness has been transferred. The properties of the cell subpopulation(s) involved in effecting the unresponsive state will be determined.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS022851-02
Application #
3405642
Study Section
Toxicology Study Section (TOX)
Project Start
1985-03-01
Project End
1988-02-29
Budget Start
1986-03-01
Budget End
1988-02-29
Support Year
2
Fiscal Year
1986
Total Cost
Indirect Cost

  Institution

Name
University of Toledo
Department
Type
Schools of Pharmacy
DUNS #
City
Toledo
State
OH
Country
United States
Zip Code
43606