Abstract

Experimental autoimmune encephalomyelitis (EAE) was induced in the susceptible SJL/J mouse strain by immunization with the myelin basic protein. Lymph node cells from these immunized mice were inoculated into nanve SJL/J mice, which induces an EAE condition that involves cycles of relapse and remission. Relapse was associated with increased IFN-g. In contrast, remission cycles were immediately preceded by peak levels of indoleamine 2,3-dioxygenase (IDO) detected in neurons but not in other tissue. IDO is an enzyme that catabolizes tryptophan, which is required for T lymphocyte survival. These results raises the possibility that IDO contributes to the remission phases of EAE (and possibly MS) by destroying specific T cells residing in nervous tissue that contribute to this autoimmune condition. Our preliminary data using longitudinal, cryopreserved blood samples from remitting and relapsing patients with multiple sclerosis suggest that IFN-g is indreased during or preceeding relapse and that IDO is aupregulated during or preceeding the remission phases. These findings may shed light on the regulatory aspects of this autoimmune disease.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
Division of Basic Sciences - NCI (NCI)
Type
Intramural Research (Z01)
Project #
1Z01BC009282-16
Application #
6762168
Study Section
(EIB)
Project Start
Project End
Budget Start
Budget End
Support Year
16
Fiscal Year
2002
Total Cost
Indirect Cost

  Institution

Name
Basic Sciences
Department
Type
DUNS #
City
State
Country
United States
Zip Code