Pathogenesis of acute passive murine encephalomyelitis II. Th1 phenotype of the inducing population is not sufficient to cause disease

The present study was designed to assess the pattern of cytokine expression over the course of disease in the central nervous system (CNS) of recipien ts of an encephalitogenic T-cell clone specific for proteolipid protein (PL P) peptide 139-151. Reverse transcriptase-polymerase chain reaction (RT-PCR ) analyses of CNS mRNA from samples taken during the onset of acute disease demonstrated upregulation of message for cytokines involved in the recruit ment and activation of macrophages (CM-CSF, interleukin (LL)-3, IL-9) and t he inflammatory cytokines tumor necrosis factor (TNF)-alpha and iNOS as wel l as message for IL-10 and transforming growth factor (TGF)beta. During the recovery stage message for most cytokines was absent, but during relapse i nflammatory cytokine messages were again detectable. Message for the access ory molecules B7-2 and CTLA-4 was observed only on the day of onset of acut e experimental allergic encephalomyelitis (EAE) and at relapse. The message s for these molecules were downregulated at the onset of recovery. These re sults illustrate the dynamic nature of the immune response during the cours e of EAE, and support a model of disease in which T-cells are involved in t he regulation of disease while a nonspecific inflammatory reaction is respo nsible for the CNS damage observed during EAE. (C) 1999 Elsevier Science B. V. All rights reserved.