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

I. M. Bronner; J. E. Hoogendijk; M. de Visser; J. Van de Vlekkert; U. A. Badrising; A. R. Wintzen; B. M. J. Uitdehaag; M. Blokland-Fromme; J. H. W. Leusen; W.-L. van der Pol; I.F. Bronner

doi:https://doi.org/10.1111/j.1399-0039.2009.01236.x

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

I. M. Bronner, J. E. Hoogendijk, M. de Visser, J. Van de Vlekkert, U. A. Badrising, A. R. Wintzen, B. M. J. Uitdehaag, M. Blokland-Fromme, J. H. W. Leusen, W.-L. van der Pol, I.F. Bronner

Research output: Contribution to journal › Article › Academic › peer-review

4 Citations (Scopus)

Abstract

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

Original language	English
Pages (from-to)	586-589
Journal	Tissue antigens
Volume	73
Issue number	6
DOIs	https://doi.org/10.1111/j.1399-0039.2009.01236.x
Publication status	Published - 2009

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https://doi.org/10.1111/j.1399-0039.2009.01236.x

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Bronner, I. M., Hoogendijk, J. E., de Visser, M., Van de Vlekkert, J., Badrising, U. A., Wintzen, A. R., Uitdehaag, B. M. J., Blokland-Fromme, M., Leusen, J. H. W., van der Pol, W.-L., & Bronner, I. F. (2009). Association of the leukocyte immunoglobulin G (Fcgamma) receptor IIIa-158V/F polymorphism with inflammatory myopathies in Dutch patients. Tissue antigens, 73(6), 586-589. https://doi.org/10.1111/j.1399-0039.2009.01236.x

@article{e1a5239d748240c9a1d4a920b702721a,

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

abstract = "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",

author = "Bronner, {I. M.} and Hoogendijk, {J. E.} and {de Visser}, M. and {Van de Vlekkert}, J. and Badrising, {U. A.} and Wintzen, {A. R.} and Uitdehaag, {B. M. J.} and M. Blokland-Fromme and Leusen, {J. H. W.} and {van der Pol}, W.-L. and I.F. Bronner",

year = "2009",

doi = "https://doi.org/10.1111/j.1399-0039.2009.01236.x",

language = "English",

volume = "73",

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Bronner, IM, Hoogendijk, JE, de Visser, M, Van de Vlekkert, J, Badrising, UA, Wintzen, AR, Uitdehaag, BMJ, Blokland-Fromme, M, Leusen, JHW, van der Pol, W-L & Bronner, IF 2009, 'Association of the leukocyte immunoglobulin G (Fcgamma) receptor IIIa-158V/F polymorphism with inflammatory myopathies in Dutch patients', Tissue antigens, vol. 73, no. 6, pp. 586-589. https://doi.org/10.1111/j.1399-0039.2009.01236.x

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T1 - Association of the leukocyte immunoglobulin G (Fcgamma) receptor IIIa-158V/F polymorphism with inflammatory myopathies in Dutch patients

AU - Bronner, I. M.

AU - Hoogendijk, J. E.

AU - de Visser, M.

AU - Van de Vlekkert, J.

AU - Badrising, U. A.

AU - Wintzen, A. R.

AU - Uitdehaag, B. M. J.

AU - Blokland-Fromme, M.

AU - Leusen, J. H. W.

AU - van der Pol, W.-L.

AU - Bronner, I.F.

PY - 2009

Y1 - 2009

N2 - 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

AB - 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

U2 - https://doi.org/10.1111/j.1399-0039.2009.01236.x

DO - https://doi.org/10.1111/j.1399-0039.2009.01236.x

M3 - Article

C2 - 19493236

SN - 0001-2815

VL - 73

SP - 586

EP - 589

JO - Tissue antigens

JF - Tissue antigens

IS - 6

ER -