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IL-1 Receptor Antagonist-Mediated Therapeutic Effect in Murine Myasthenia Gravis Is Associated with Suppressed Serum Proinflammatory Cytokines, C3, and Anti-Acetylcholine Receptor IgG1¹

Huan Yang^2,*, Erdem Tüzün^*, Dhivyaa Alagappan^*, Xiang Yu, Benjamin G. Scott^*, Alexander Ischenko and Premkumar Christadoss^3,*

^* Department of Microbiology and Immunology, and Department of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555; and Institute of Highly Pure Biopreparations, St. Petersburg, Russia

In myasthenia gravis (MG), TNF and IL-1 polymorphisms and high serum levels of these proinflammatory cytokines have been observed. Likewise, TNF and IL-1 are critical for the activation of acetylcholine receptor (AChR)-specific T and B cells and for the development of experimental autoimmune myasthenia gravis (EAMG) induced by AChR immunization. We tested the therapeutic effect of human recombinant IL-1 receptor antagonist (IL-1ra) in C57BL/6 mice with EAMG. Multiple daily injections of 0.01 mg of IL-1ra administered for 2 wk following two AChR immunizations decreased the incidence and severity of clinical EAMG. Furthermore, IL-1ra treatment of mice with ongoing clinical EAMG reduced the clinical symptoms of disease. The IL-1ra-mediated suppression of clinical disease was associated with suppressed serum IFN-, TNF-, IL-1, IL-2, IL-6, C3, and anti-AChR IgG1 without influencing total serum IgG. Therefore, IL-1ra could be used as a nonsteroidal drug for the treatment of MG.

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