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Neurology 1999;52:1771
© 1999 American Academy of Neurology
Articles

Immunoglobulin G Fc-receptor (Fc{gamma}R) IIA and IIIB polymorphisms related to disability in MS

Kjell-Morten Myhr, MD, Guttorm Raknes, MS, Harald Nyland, MD, PhD and Christian Vedeler, MD, PhD

From the Department of Neurology, Haukeland Hospital, University of Bergen, Norway.

Address correspondence and reprint requests to Dr K.-M. Myhr, Department of Neurology, Haukeland Hospital, N-5021 Bergen, Norway; e-mail: Kjell.M.Myhr{at}nevro.haukeland.no

OBJECTIVE: MS is immunologically mediated in genetically susceptible individuals. Receptors for the Fc fragment of immunoglobulin G (IgG) (Fc{gamma}R) link the humoral and cellular immune responses by targeting immune complexes to effector cells. Different Fc{gamma}R show variability in their distribution, strength, and capacity of binding different IgG subclasses.

METHODS: To investigate the role of Fc{gamma}R in MS, 136 MS patients and 96 matched controls were genotyped for Fc{gamma}RIIA and Fc{gamma}RIIIB gene polymorphisms; the results were correlated to disease susceptibility and severity measured by the Expanded Disability Status Scale (EDSS).

RESULTS: The allele frequencies of the Fc{gamma}RIIA and Fc{gamma}RIIIB did not differ significantly between the MS patients and the controls. Patients homozygous for the Fc{gamma}RIIIB neutrophil antigen (NA) 1 allele had a significantly more benign course of MS than patients heterozygous or homozygous for the Fc{gamma}RIIIB NA2 allele. Patients homozygous for the Fc{gamma}RIIA histidine (H) allele also had a more benign course of MS than patients heterozygous or homozygous for the Fc{gamma}RIIA arginine (R) allele.

CONCLUSION: The results implicate Fc{gamma}RIIIB and to a lesser extent Fc{gamma}RIIA as disease-modifying genes in MS. Fc{gamma}RIIIB NA1/NA1 and Fc{gamma}RIIA H/H bind more efficient IgG1/IgG3 and IgG2 subclasses, respectively, than Fc{gamma}RIIIB NA2/NA2 and Fc{gamma}RIIA R/R. A more effective processing of circulating immune complexes may be one mechanism for better clinical outcome in MS.




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