Thalidomide prolongs experimental autoimmune neuritis in Lewis rats
| Autor: | Hans Link, Jie Zhu, K Zwingenberger, Asim Diab, Moiz Bakhiet, Guo-Min Deng |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
medicine.medical_treatment
Immunology Neuritis Interferon-gamma medicine Animals Myelin Sheath Autoimmune disease Systemic lupus erythematosus business.industry General Medicine Immunotherapy medicine.disease Neuritis Autoimmune Experimental Rats Thalidomide medicine.anatomical_structure Rats Inbred Lew Cattle Bone marrow Sciatic nerve business Polyneuropathy Immunosuppressive Agents medicine.drug |
| Zdroj: | Scandinavian journal of immunology. 48(4) |
| ISSN: | 0300-9475 |
| Popis: | 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-Barre 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. |
| Databáze: | OpenAIRE |
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