Association of the leukocyte immunoglobulin G (Fcgamma) receptor IIIa-158V/F polymorphism with inflammatory myopathies in Dutch patients.

Authors: Bronner, IM  Hoogendijk, JE  De Visser, M  Van de Vlekkert, J  Badrising, UA  Wintzen, AR  Uitdehaag, BM  Blokland-Fromme, M  Leusen, JH  Van der Pol, WL 
Citation: Bronner IM, etal., Tissue Antigens. 2009 Jun;73(6):586-9.
Pubmed: (View Article at PubMed) PMID:19493236
DOI: Full-text: DOI:10.1111/j.1399-0039.2009.01236.x

Leukocytes are involved in the pathogenesis of idiopathic inflammatory myopathies (IIMs). Immunoglobulin G (IgG) receptors (FcgammaR) link the specificity of IgG to the effector functions of leukocytes. Several FcgammaR subclasses display functional polymorphisms that determine in part the vigour of the inflammatory response. FcgammaRIIIa genotypes were differentially distributed among 100 IIM patients compared with 514 healthy controls with a significant increase of the homozygous FcgammaRIIIa-V-158 genotype (3 x 2 contingency table, chi(2) = 6.3, P = 0.04). Odds ratios (ORs) increased at the addition of each FcgammaRIIIa-V-158 allele, in particular among patients with non-specific myositis and dermatomyositis {OR 2.1 [95% confidence interval (CI) 1.1-4.3] and 2.7 (95% CI 1.1-6.4) for FcgammaRIIIa-V/F158 and FcgammaRIIIa-V/V158 genotypes, respectively, using FcgammaRIIIa-F/F158 as a reference group}. These data suggest that the FcgammaRIIIa-V-158 allele may constitute a genetic risk marker for IIM.


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Created: 2011-10-17
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