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Severity of Guillain–Barré syndrome is associated with Fcγ Receptor III polymorphisms

2005; Elsevier BV; Volume: 162; Issue: 1-2 Linguagem: Inglês

10.1016/j.jneuroim.2005.01.016

1872-8421

Nina M. van Sorge, W. Ludo van der Pol, Marc Jansen, Karin Geleijns, Sandra Kalmijn, Richard AC Hughes, Jeremy Rees, Jane Pritchard, Christian A. Vedeler, Kjell‐Morten Myhr, Christopher E. 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,

T-cell and B-cell Immunology

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.