| Literature DB >> 15833371 |
Nina M van Sorge1, 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.
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.Entities:
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Year: 2005 PMID： 15833371 DOI： 10.1016/j.jneuroim.2005.01.016
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478