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Neurology 2000;54:1661-1665
© 2000 American Academy of Neurology
Articles

IgG receptor IIa alleles determine susceptibility and severity of Guillain-Barré syndrome

W.-L. van der Pol, MD, L. H. van den Berg, MD, R. H. M. Scheepers, MSc, J. G. van der Bom, MD, P. A. van Doorn, MD, R. van Koningsveld, MD, M. C. L. van den Broek, MD, J. H. J. Wokke, MD and J. G. J. van de Winkel, PhD

From the Departments of Immunology (Drs. van der Pol, Scheepers, and van de Winkel) and Neurology (Drs. van den Berg, van den Broek, and Wokke), Julius Centre for Patient Oriented Research (Dr. van der Bom), University Hospital Utrecht; and Department of Neurology Dijkzigt University Hospital Rotterdam (Drs. van Doorn and van Koningsveld), the Netherlands.

Address correspondence and reprint requests to Dr. Leonard H. van den Berg, Department of Neurology, University Hospital Utrecht, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands; e-mail: L.H.vandenBerg{at}neuro.AZU.nl

OBJECTIVE: Guillain-Barré syndrome (GBS) is characterized by nerve infiltration of leukocytes and autoantibodies of the immunoglobulin G (IgG) isotype directed against nerve constituents. Leukocyte receptors for IgG (Fc{gamma}R) constitute an important link between the humoral and cellular parts of the immune system and confer potent cellular effector functions to myelin-directed antibodies. Three Fc{gamma}R subclasses exhibit genetically determined biallelic functional polymorphisms (Fc{gamma}RIIa: R131 versus H131; Fc{gamma}RIIIa: 158V versus 158F; Fc{gamma}RIIIb: NA1 versus NA2) that determine efficacy of the cellular immune response. To study the relevance of these polymorphisms for susceptibility and severity of GBS, we compared Fc{gamma}R genotype distributions in GBS patients with those in controls.

METHODS: Genomic DNA was isolated from whole blood of 31 randomly selected patients with GBS and 187 healthy blood donors. Genotypes of the three polymorphic Fc{gamma}R genes were determined by PCR.

RESULTS: Fc{gamma}RIIa-H131 homozygosity was significantly increased in patients as compared with healthy controls (OR 2.45; 95% CI 1.12 to 5.36; p = 0.037). Furthermore, Fc{gamma}RIIa-H131 homozygous GBS patients had a higher risk for severe disease than did patients with other genotypes (OR 18.57; 95% CI 1.95 to 176.49; p = 0.007).

CONCLUSION: Fc{gamma}RIIa allotypes capable of initiating efficient cellular effector functions are associated with increased risk for GBS and a more severe disease course. Fc{gamma}R alleles may constitute novel genetic risk markers for GBS.

Key words: Guillain-Barré syndrome—Fc{gamma}R alleles—Polymorphism.




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