Ciclosporin A prevents P2 T cell line-mediated experimental autoimmune neuritis (AT-EAN) in rat.
Adoptive transfer experimental autoimmune neuritis (AT-EAN) produced in Lewis rats by injection of P2-reactive T lymphocyte line cells offers the unique possibility to study the exclusive contribution of cell-mediated immune responses to the pathogenesis of autoimmune disease of the peripheral nervous system (PNS). It further lends itself to the evaluation of novel therapeutic approaches that may bear relevance to the human acute Guillain-Barré syndrome. The effects of the immunosuppressive agent ciclosporin A on the clinical, electrophysiological and morphological expression of AT-EAN were examined. We found that ciclosporin A suppressed development of the disease. In view of the known actions of ciclosporin A on T cells, these results indicate the requirement of activation and clonal proliferation of T lymphocytes to produce myelin damage in autoimmune diseases of the PNS.
D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D002460:Cell Line; D003524:Cyclosporins / Q000627:therapeutic use*; D004594:Electrophysiology; D005260:Female; D004676:Myelin Basic Protein / Q000494:pharmacology*; D018996:Myelin P2 Protein; D009444:Neuritis, Autoimmune, Experimental / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D051381:Rats; D011917:Rats, Inbred Lew; D013601:T-Lymphocytes / Q000187:drug effects / Q000502:physiology*
D003524:Cyclosporins; D004676:Myelin Basic Protein; D018996:Myelin P2 Protein