“…The process of spontaneous recovery is not yet fully understood and many factors have been postulated to play a role, including endogenous corticosteroids MacPhee et al, 1989), suppressor cells (Swierkosz and Swanborg, 1975;Welch et al, 1980) and nitric oxide (O'Brien et al, 1999). Furthermore, during clinical recovery there is apoptosis of inflammatory cells in the CNS (Pender et al, 1991), which involves T cells (Pender et al, 1992;Schmied et al, 1993), B cells (White et al, 2000), macrophages (Nguyen et al, 1994;White et al, 1998a) and microglia (White et al, 1998a) and After recovery from an episode of actively induced EAE, Lewis rats have generally been found to be resistant to the active reinduction of disease (Willenborg, 1979;Hinrichs et al, 1981) and either resistant or susceptible (Willenborg, 1979;Hinrichs et al, 1981) to passively induced EAE. Rats that have recovered from passively induced EAE have been found by some authors to be fully susceptible to the active or passive reinduction of disease (Hinrichs et al, 1981) and by others to be resistant to reinduction by active (Welch et al, 1980;Namikawa et al, 1986) or passive means (Levine et al, 1967).…”