In the paralytic autoimmune disease, multiple sclerosis (MS), APC residing within the central nervous system (CNS) are required for inflammation mediated by myelin-specific T lymphocytes. Some CNS-resident APC develop from bone marrow hematopoietic progenitor cells but mechanisms controlling this process are not well understood. The development of susceptibility to experimental autoimmune encephalomyelitis (EAE) following transfer of T-depleted rat bone marrow cells (T-dBMC) was examined in SCID mice to determine the minimal time frame and conditions required for CNS population by functional, hematopoietic-derived APC. Acute paralysis, CNS inflammation and recovery were induced by activated rat T cells in SCID mice 9 days after transfer of T-dBMC. Following recovery, a second, more severe episode of paralysis was induced by T cells alone. Secondary disease was associated with proportionally more T cells and fewer bone marrow-derived cells in the CNS than primary disease. These results demonstrate that the clinical course of autoimmune disease mediated by myelin-specific T cells may be controlled by mechanisms regulating development of hematopoietic-derived APC.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology