Transfer of suboptimal numbers of EAE-effector cells can suppress acute EAE induced by myelin basic protein but leads to chronic EAE when challenged with whole CNS tissue.
Urges antigen- and dose-specific caution in EAE cell-transfer models; leaves open translation to human neuroautoimmune therapies.
Experimental allergic encephalomyelitis (EAE) in strain 13 guinea pigs is an acute monophasic disease induced with myelin basic protein (BP) in complete Freund's adjuvant (CFA). We report here that EAE can be effectively suppressed by transfer of a limited number of EAE-effector cells. Lymph node cells (LNC) from donors sensitized with BP/CFA are activated in vitro by incubation with BP and strain 2 peritoneal exudate cells (PEC). 5 X 10(7) of these cells are capable of inducing lethal EAE in recipients; 0.5 to 1 X 10(7) cells (a suboptimal transfer) effectively suppress EAE induction in animals subsequently sensitized with BP/CFA. Suppressed recipients develop an early mild disease from which they recover completely. In contrast, suboptimal transfer of BP-sensitized cells does not protect recipients against sensitization with whole central nervous system (CNS) tissue/CFA. About 50% of these recipients succumb to acute EAE; the survivors develop chronic EAE of varying intensity: a mild chronic form with recovery, a severe chronic form that is eventually fatal, and a chronic relapsing form that results in permanent neurologic deficit. Preliminary attempts at detecting suppressor cells in the suppressed animals were unsuccessful. Instead, PEC of all recipients of suboptimal transfers were capable of transferring EAE to naive animals.
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Driscoll et al. (1982) studied this question.
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