Modulation by cyclosporin-A of mononuclear cell distribution during experimental allergic encephalomyelitis.
The capacity of CS-A to modify some inflammatory aspects of a cell mediated disease process, has been studied. In the present work, CS-A was shown to be effective at two levels during the development of experimental allergic encephalomyelitis (EAE) in rats. If CS-A was given at the time of the induction of the disease it inhibited lymphocyte proliferation in vivo, lymphocyte trapping into the draining lymph nodes, and delayed the subsequent infiltration of cells into the CNS and other inflammatory sites. When given around the time of disease manifestation, CS-A also reduced the rate of cell accumulation into the CNS and foot, but was without effect in modifying lymphocyte trapping in the draining nodes, despite the fact that this was still an ongoing process. Clinical signs were similarly delayed or reduced by both regimen of CS-A treatment. Treatment with CS-A did not lead, however, to long lasting unresponsiveness, since both treated groups suffered a relapse of disease at various times after treatment had been discontinued.
D000818:Animals; D002490:Central Nervous System; D003524:Cyclosporins / Q000494:pharmacology*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000473:pathology; D005260:Female; D005528:Foot; D008198:Lymph Nodes / Q000473:pathology; D008213:Lymphocyte Activation / Q000187:drug effects; D008214:Lymphocytes / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D009000:Monocytes / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D051381:Rats; D011917:Rats, Inbred Lew
D003524:Cyclosporins