THE EFFECT OF PROTECTING GUINEA‐PIGS AGAINST EAE ON THE MENINGEAL INFLAMMATORY CELL‐INFILTRATE

Abstract

Allsopp G., Parker D. & Turk J.L. (1981) Neuropathology and Applied Neurobiology 7, 477–487 The effect of protecting guinea-pigs against EAE on the meningeal inflammatory cell infiltrate Guinea-pigs were found to be fully protected from the clinical signs of EAE when they were given spinal cord in FIA either 3, 7 or 14 days before immunization with spinal cord in FCA. If the animals were protected by the recruitment of suppressor cells then cyclophosphamide (CY) might break this protection. CY at 300 mg/kg) and 20 mg/kg was given either before the protective inoculum to try to eliminate suppressor cell precursors or before immunization to eliminate the suppressor cells themselves. No clinical signs of EAE developed in any of these groups of guinea-pigs. It was found, however, that large numbers of meningeal inflammatory cells could be isolated from the brains of guinea-pigs protected from EAE when the protective inoculum was given only 1 week before immunization. These cell numbers were further significantly increased by giving CY in addition to the protective inoculum. The meningeal inflammatory cells and peritoneal exudate cells (PECs) from guinea-pigs protected against EAE were compared to those isolated from animals with acute EAE. These cells from guinea-pigs with acute EAE responded, in the lymphocyte transformation test, to the mitogen. The PECs also responded to the brain antigen, myelin basic protein (MBP) and to tuberculin (PPD). The meningeal inflammatory cells did not respond to either antigen. The PECs from animals protected against EAE responded to mitogen and PPD, but not to MBP, but the meningeal inflammatory cells did not respond to antigen or mitogen. The percentage of T lymphocytes in the meningeal inflammatory infiltrates of protected and unprotected guinea-pigs was similar, but that of phagocytic cells was significantly depressed in the inflammatory infiltrates of animals protected against EAE.