Experimental allergic encephalomyelitis (EAE), an animal model for multiple sclerosis (MS), is a paralytic disease of the central nervous system (CNS) mediated by T‐lymphocytes reactive to myelin basic protein (MBP). Lewis rats actively immunized with fragment 68 to 82 of guinea pig MBP develop a monophasic disease with spontaneous recovery. Lymphocyte recognition of the primary encephalitogenic sequence of MBP (fragment 68 to 82) is Vβ8.2 T cell receptor (TCR) skewed [1–3]. Lewis rats in clinical remission at 1 month and 3 months after spontaneous resolution of EAE retain Vβ8.2 T‐lymphocytes in the CNS when analyzed by reverse transcriptase polymerase chain reaction or in situ hybridization. In contrast, I and 3 months after clinical remission from syngeneic bone marrow transplantation, Vβ8.2 T lymphocytes are absent from the CNS. During clinically active EAE and inflammatory breakdown of the blood‐brain barrier, immune ablation and reconstitution with syngeneic bone marrow results in clinical tolerance of the new immune system to myelin. © 1995 Wiley‐Liss, Inc.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Neuroscience Research|
|State||Published - Jul 1 1995|
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience