Photo Credit: iStock.com/CreVis2
FCGR3A duplications may worsen Guillain-Barré syndrome in cases linked to C. jejuni.
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 (FcγRs), may contribute to the development of Guillain-Barré syndrome (GBS).
Researchers investigated whether genetic variation in the FCGR2/3 locus influenced susceptibility, muscle weakness, clinical outcomes, and intravenous immunoglobulin (IVIg) pharmacokinetics in GBS.
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
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 higher frequency of FCGR3A copy number ≥3 was found compared to controls (P= 0.023). Increased FCGR3A copy numbers were also associated with severe weakness [OR= 2.02; 95% CI= 1.00–4.12], 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.
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–related cases.
Source: link.springer.com/article/10.1007/s00415-025-13216-8