We investigated the expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) by cells in the central nervous system (CNS) of Lewis rats during acute experimental allergic encephalomyelitis (EAE). A few endothelial cells in the CNS of normal rats expressed ICAM-1, whereas during the active phase of EAE, ICAM-1 was present on many endothelial cells. This alteration was detectable the day before clinical symptoms. Sincc histopathological studies showed few detectable mononuclear cells or inflammatory foci in any section of the preclinical rats, the expression of ICMA-1 was considered to be important at least in the early stage of inflammation. LFA-1 was seen on perivascular infiltrating cells. An increase in either ICAM-1- or LFA-1-positive cells was initially seen in the lumbosacral portion of the spinal cord, which then extended to the thoracic portion. The number of either ICAM-1- or LFA-1-positive cells peaked on the day of clinical onset in the lumbosacral portion. In contrast, in the thoracic portion, a peak in the number of either ICAM-1- or LFA-1-positivc cells was observed on the day after clinical onset. This ascending extension of either ICAM-1- or LFA-1-positive cells was correlated with the progression of neurologic signs. It is suggested that increased expression of ICAM-1 and LFA-1 in the CNS of rat EAE may promote the extravasation of lymphocytes across the blood-brain barrier and be related to progression of the disease.