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Absence of antibodies to glutamate receptor type 3 (GluR3) in Rasmussen encephalitis

From the Neurosciences Group (Drs. Beeson, Vincent, and Lang, R. Watson, Y. Jiang, L. Clover, and K. McKnight), Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, and Department of Clinical Neurology (Drs. Y. Hart and Palace), Radcliffe Infirmary, University of Oxford, UK; School of Biomedical Sciences (Dr. Bermudez, L. Houlihan), Oxford Brookes University, UK; Neurosciences Unit (J.H. Cross), Institute of Child Health & Great Ormond Street Hospital for Children NHS Trust, London, UK; University Department of Neurological Sciences (Dr. I.K. Hart), Walton Centre, Liverpool, UK; and INSERM U-583 (Drs. Roubertie and Valmier), Institut des Neurosciences de Montpellier, Université Montpellier II, France.

Address correspondence and reprint requests to Dr. Bethan Lang, Neurosciences Group, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, OX3 9DS, UK; e-mail: blang{at}hammer.imm.ox.ac.uk

Objective: To determine the prevalence of serum antibodies to the ionotropic glutamate receptor 3 (GluR3) in patients with Rasmussen encephalitis (RE), a severe epileptic disorder, and to compare with serum from control subjects and patients with intractable epilepsy (IE).

Methods: The authors looked for serum immunoglobulin (Ig) G antibodies to GluR3 in 30 patients with RE, including two patients who had plasma exchange and 12 who had been treated with IV Igs with varying results, and 49 patients with IE and 23 healthy individuals, using ELISA with GluR3B peptide, Western blot analysis of recombinant full-length GluR3, immunoprecipitation of [³⁵S]- and [¹²⁵I]-labeled GluR3 extracellular domains, immunohistochemistry on rat brain sections, and electrophysiology of GluR3 expressed in Xenopus oocytes.

Results: Low levels of antibodies to the GluR3B peptide were detected using ELISA in only 4 of the 79 patients with epilepsy (2 with RE and 2 with IE); binding to GluR3B in other sera was shown to be nonspecific. One other patient with IE had antibodies to recombinant GluR3 on Western blot analysis. However, none of the sera tested precipitated either the [³⁵S]- or the [¹²⁵I]-labeled GluR3 domains; none bound to rat brain sections in a manner similar to rabbit antibodies to GluR3; and none of the nine sera tested affected the electrophysiologic function of GluR3.

Conclusions: GluR3 antibodies were only infrequently found in Rasmussen encephalitis or intractable epilepsy.

Received October 2, 2003. Accepted in final form February 25, 2004.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the July 13 issue to find the title link for this article.

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