Recipient contributions to serial passive transfer of experimental allergic encephalomyelitis

EAE can be adoptively transferred into normal recipients by the transfer of BP-specific EAE effector cells. After cell transfer, a series of ill-defined events occur in the recipient that culminate in the development of paralysis associated with neural tissue damage. We investigated the subsequent recipient response to the adoptively transferred disease and examined the role that recipient lymphocytes play in the development of adoptively transferred EAE. Recipient involvement was assessed by the transfer of EAE through a series of normal F1 animals as recipients and at the endpoint of the experiment, determining the MHC restriction pattern of the BP-sensitive cells present. The serial transfer of EAE from BP-CFA-sensitized LEW----(LEW X F-344)F1----(LEW X P2)F1, and from BP-CFA sensitized LEW----(LEW X F344)F1----(LEW X F-344)F1, resulted in the development of BP-sensitive cells in the spleens of the secondary recipients that were able to transfer disease into normal LEW recipients. To test directly for the development of host-derived BP-sensitive cells that might arise in the F1 animal, the serial transfer of EAE from LEW----(LEW X ACI)F1----(LEW X ACI)F1 was performed. When BP-sensitive cells obtained from the secondary (LEW X ACI)F1 recipient animal were transferred into either normal LEW and ACI, or irradiated LEW and ACI animals as final recipients, transfer of disease was successful only into the LEW parental. These results suggest that the development of passive EAE is due solely to the transferred BP-sensitive cells originating from the actively immunized donor, and that no host-derived lymphocytes are recruited into the pool of EAE effector precursor cells found in the spleen of animals after the development of adoptively transferred EAE.