Severity of Guillain-Barré syndrome is associated with Fc gamma Receptor III polymorphisms

Nina M. van Sorge, W.-Ludo van der Pol, Marc D. Jansen, Karin P. W. Geleijns, Sandra Kalmijn, Richard A. C. Hughes, Jeremy H. Rees, Jane Pritchard, Christian A. Vedeler, Kjell-Morten Myhr, Chris Shaw, Ivo N. van Schaik, John H. J. Wokke, Pieter A. van Doorn, Bart C. Jacobs, Jan G. J. van de Winkel, Leonard H. van den Berg

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Abstract

Macrophages and ganglioside-specific IgG are involved in the pathogenesis of Guillain-Barre syndrome (GBS). Leukocyte IgG receptors (Fc gammaR) confer potent cellular effector functions to the specificity of IgG. The efficacy of IgG-mediated cellular inflammatory responses is determined by functional polymorphisms of three Fc gammaR subclasses (Fc gammaRIIa: H131/R131; Fc gammaRIIIa: V158/F158; Fc gammaRIIIb: NA1/NA2). Fc gammaR genotype distributions were determined in a Dutch, and British cohort of GBS patients and controls. In addition, a meta-analysis incorporating all previously published data, encompassing a total of 345 GBS patients and 714 healthy controls, was performed. Results suggest that Fc gammaRIII genotypes may represent mild disease-modifying factors in GBS
Original languageEnglish
Pages (from-to)157-164
JournalJournal of Neuroimmunology
Volume162
Issue number1-2
DOIs
Publication statusPublished - 2005

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