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R) IIA and IIIB polymorphisms related to disability in MS
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
R) link the humoral and cellular immune responses by targeting immune complexes to effector cells. Different FcR show variability in their distribution, strength, and capacity of binding different IgG subclasses.
METHODS: To investigate the role of FcR in MS, 136 MS patients and 96 matched controls were genotyped for FcRIIA and FcRIIIB 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 FcRIIA and FcRIIIB did not differ significantly between the MS patients and the controls. Patients homozygous for the FcRIIIB neutrophil antigen (NA) 1 allele had a significantly more benign course of MS than patients heterozygous or homozygous for the FcRIIIB NA2 allele. Patients homozygous for the FcRIIA histidine (H) allele also had a more benign course of MS than patients heterozygous or homozygous for the FcRIIA arginine (R) allele.
CONCLUSION: The results implicate FcRIIIB and to a lesser extent FcRIIA as disease-modifying genes in MS. FcRIIIB NA1/NA1 and FcRIIA H/H bind more efficient IgG1/IgG3 and IgG2 subclasses, respectively, than FcRIIIB NA2/NA2 and FcRIIA R/R. A more effective processing of circulating immune complexes may be one mechanism for better clinical outcome in MS.
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