Summary: Passive transfer of living lymph node cells from donor rats with experimental allergic encephalomyelitis (EAE) to normal isologous recipients caused clinical signs of EAE after 3 to 7 days. Large doses of cells, or adrenalectomy of recipients, advanced the onset of clinical disease to 2 days after transfer. The combination of large doses of cells and adrenalectomy of recipients reduced the incubation period to 24 hr. There was an exponential relationship between dose of cells and incubation period in adrenalectomized recipients, possibly reflecting mitotic division of donor cells during the latent period. Lesions of EAE produced by passive transfer localized in and around areas of the brain damaged by cyanide, as has been reported previously for EAE produced by active sensitization. Donor cells immunized against either isologous or heterologous central nervous system (CNS) antigens were effective. Localization was best when the cyanide was administered 1 to 4 days before the transfer. EAE was not produced when heat-killed encephalitogenic cells or living, stimulated but non-encephalitogenic cells were injected into cyanide-treated recipients, even when nonencephalitogenic cells were combined with serum from rats with EAE. Cyanide damage lowered the threshold for passively transferred EAE, probably due to reduction of the blood-brain barrier and/or increased accessibility of CNS antigens. Brain lesions caused by passive transfer of EAE to cyanide-treated recipients were detectable at 6 hr, well developed at 10 hr and maximal at 24 hr. This rate of lesion development was similar to that reported by others for development of delayed hypersensitivity reactions following passive transfer of tuberculin sensitized cells and separate, simultaneous injection of tuberculin. Because transferred cells are temporarily retained in the pulmonary filter, and because this obstacle was not overcome by injection into the carotid artery, it is likely that these results are close to the presently attainable limit for speed of detection of passive transfer of EAE.