02039nas a2200301   4500000000100000008004100001260001300042653001200055653001100067653002900078653002100107653001800128653003900146653000900185653002100194653001600215100001000231700001300241700001100254700002000265700001400285700001100299245007300310300001200383490000700395520132100402022001401723       1998                            d  c1998 Oct10aAnimals10aCattle10aImmunosuppressive Agents10aInterferon-gamma10aMyelin Sheath10aNeuritis, Autoimmune, Experimental10aRats10aRats, Inbred Lew10aThalidomide1 aZhu J1 aDeng G M1 aDiab A1 aZwingenberger K1 aBakhiet M1 aLink H00aThalidomide prolongs experimental autoimmune neuritis in Lewis rats.  a397-4020 v483 a<p>Thalidomide is reported to have immunomodulatory and anti-inflammatory effects, which have led to its use in the treatment of a number of immune-mediated disorders, including leprosy, discoid lupus and Behcet's disease, and to prevent immunological rejection phenomena following skin and bone marrow grafts. Experimental autoimmune neuritis (EAN) is a CD4+ T-cell-mediated demyelinating autoimmune disease, which represents an animal model for the study of the immunopathogenesis and immunotherapy of Guillain-Barré syndrome (GBS) in humans. We examined the effect of thalidomide in Lewis rats with EAN, which was induced by immunization with bovine peripheral nerve myelin (BPM) and complete Freund's adjuvant (CFA). Thalidomide prolonged clinical EAN when given at a dose of 200 mg/kg/day by gavage. This clinical effect was associated with increased numbers of inflammatory cells in sciatic nerve sections and elevated numbers of interferon-gamma (IFN-gamma) mRNA-expressing cells among lymph node mononuclear cells from thalidomide-treated EAN rats on day 17 postimmunization, i.e. at the peak of clinical EAN. The finding that thalidomide prolongs clinical EAN is in agreement with the clinical polyneuropathy reported in patients receiving treatment with thalidomide and limits its clinical usefulness.</p>  a0300-9475