Cited 37 times since 2005 (1.8 per year) source: EuropePMC Journal of neuroimmunology, Volume 162, Issue 1-2, 1 1 2005, Pages 157-164 Severity of Guillain-Barré syndrome is associated with Fc gamma Receptor III polymorphisms. van Sorge NM, van der Pol WL, Jansen MD, Geleijns KP, Kalmijn S, Hughes RA, Rees JH, Pritchard J, Vedeler CA, Myhr KM, Shaw C, van Schaik IN, Wokke JH, van Doorn PA, Jacobs BC, van de Winkel JG, van den Berg LH
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.
