Photo Credit: iStock.com\/CreVis2<\/p>\n
FCGR3A duplications may worsen Guillain-Barr\u00e9 syndrome in cases linked to C. jejuni.\u00a0\u00a0<\/p>\n
A study published in July 2025 issue of Journal of Neurology explored how genetic variability in the FCGR2\/3 locus, which encodes low-to-medium-affinity Fc-gamma receptors (Fc\u03b3Rs), may contribute to the development of Guillain-Barr\u00e9 syndrome (GBS).\u00a0\u00a0<\/p>\n
Researchers investigated whether genetic variation in the FCGR2\/3 locus influenced susceptibility, muscle weakness, clinical outcomes, and intravenous immunoglobulin (IVIg) pharmacokinetics in GBS.\u00a0\u00a0<\/p>\n
They analyzed copy number variation and single nucleotide polymorphisms in the FCGR2\/3 locus using multiplex ligation-dependent probe amplification (MLPA). The study included 467 individuals with GBS and 919 healthy controls of European descent. Severe muscle weakness was defined by a Medical Research Council (MRC) sum score of less than 40 at nadir [MRC sum score\u2009\u00a0<\/p>\n
The results showed that no significant link was observed between FCGR2\/3 genetic variation and GBS susceptibility. Among individuals with prior Campylobacter jejuni infection<\/a>, a higher frequency of FCGR3A copy number \u22653 was found compared to controls (P=\u20090.023). Increased FCGR3A copy numbers were also associated with severe weakness [OR=\u20092.02; 95% CI=\u20091.00\u20134.12], independent of age and C. jejuni serology. No correlation was noted between FCGR2\/3 variants and recovery of unaided walking in time-to-event analysis. Additionally, FCGR2\/3 genetic variation did not influence IVIg pharmacokinetics.\u00a0\u00a0<\/p>\n Investigators concluded that FCGR2\/3 polymorphisms were not linked to GBS susceptibility or IVIg response, though subgroup analysis revealed an association between FCGR3A duplication and Campylobacter jejuni\u2013related cases.\u00a0<\/p>\n