Pegylated interferon induced myasthenia crisis--a case report.
Congeni Jonathan P,Kirkpatrick Robert B
Journal of clinical neuromuscular disease
Interferons (IFNs) have antiviral, antimitogenic, and immunostimulatory effects and are often used in the treatment of viral hepatitis and some neoplasms. Combination pegylated IFN-alpha and ribavirin therapy is currently recommended for the treatment of hepatitis C. Triple therapy, with the addition of a protease inhibitor, such as telaprevir or boceprevir, has recently become a mainstay of therapy for certain genotypes. There have also been reports outlining side effects associated with conventional IFN therapy and its immunostimulatory effects, which may cause autoimmune phenomena, including but not limited to Guillain-Barre syndrome, polymyositis, acute and chronic demyelinating polyneuropathy, and myasthenia gravis. Although a number of cases of interferon-induced myasthenia gravis have been reported, we present a case of interferon-induced myasthenia crisis that developed soon after retreatment of hepatitis C with combination interferon, ribavirin, and telaprevir.
[A case of thymoma-associated myasthenia gravis with antibodies against interferon-alpha--a clinico-immunological follow up of the symptoms and its titer].
Nakamori Masayuki,Matsumura Tsuyoshi,Saito Toshio,Kunitomi Atsuhiro,Iyama Akinori,Nozaki Sonoko,Fujimura Harutoshi,Shinno Susumu
Rinsho shinkeigaku = Clinical neurology
A 73-year-old woman developed myasthenia gravis (MG) with thymoma. She had a very high level of serum antibodies against interferon-alfa (IFN-alpha). We observed the changes to her clinical symptoms and titer of the antibody during therapeutic course. Although she underwent thymectomy, intravenous methylprednisolone therapy, and oral tacrolimus administration, MG symptoms of the patient were not significantly improved and the antibody titer remained at a high level. IFN-alpha is a potent immunomodulating cytokine that regulates MHC class II expression on antigen presenting cells and activities of NK cells, B cells, and helper/suppressor T cells. This case suggests that IFN-alpha related immunological perturbation participates in the pathogenesis of thymoma-associated myasthenia gravis.
Progression of type 1 diabetes from the prediabetic stage is controlled by interferon-α signaling.
Marro Brett S,Ware Brian C,Zak Jaroslav,de la Torre Juan Carlos,Rosen Hugh,Oldstone Michael B A
Proceedings of the National Academy of Sciences of the United States of America
Blockade of IFN-α but not IFN-β signaling using either an antibody or a selective S1PR1 agonist, CYM-5442, prevented type 1 diabetes (T1D) in the mouse -LCMV T1D model. First, treatment with antibody or CYM-5442 limited the migration of autoimmune "antiself" T cells to the external boundaries around the islets and prevented their entry into the islets so they could not be positioned to engage, kill, and thus remove insulin-producing β cells. Second, CYM-5442 induced an exhaustion signature in antiself T cells by up-regulating the negative immune regulator receptor genes , and , thereby limiting their killing ability. By such means, insulin production was preserved and glucose regulation maintained, and a mechanism for S1PR1 immunomodulation described.