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Comment on ‘No association of primary Sjögren’s syndrome with Fcγ receptor gene variants’

Genes & Immunity volume 14, pages 530–531 (2013)Cite this article

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The article by Haldorsen et al.1 describes a genetic association study for primary Sjögren’s syndrome (pSS), and the FCGR gene cluster on Chr1q22. The study evaluated both genomic copy number variation (CNV) in the FCGR3B gene, and four single-nucleotide polymorphisms (SNPs) in FCGR2A, FCGR3A and FCGR3B, respectively. No associations were observed.

Copy number variation has been identified in multiple genes in the FCGR gene cluster,2 but perhaps the best characterized in FCGR3B. Individuals may carry 0, 1, 2, 3 or 4 copies of FCGR3B, indicating that a single chromosome may carry a deletion or a duplication of the gene. In recent years, a convincing body of evidence has accumulated demonstrating that low FCGR3B copy number (that is, 0 or 1 copy, or carriage of a FCGR3B deletion on at least one chromosome) is associated with susceptibility to systemic autoimmune disease (reviewed in the study by McKinney and Merriman3), and in particular, systemic lupus erythematosus (SLE). As there is considerable clinical, serological and genetic overlap between SLE and pSS, characterization of the association between low FCGR3B and pSS is of great interest. While the Haldorsen et al.1 study, which examined FCGR3B CNV in Norwegian pSS patients, was negative, two previously published studies have both reported an association between low FCGR3B copy number and pSS in American4 and Australian5 cohorts, and we were the authors of this latter study. Haldorsen et al.1 suggest that the discrepancy between our two studies is due to technical superiority of their study (in terms of a small difference in the stringency of the allowable standard deviation of the replicate ΔCq values), or the fact that our controls were not gender matched (without providing a rationale for suggesting there will be a gender difference in autosomal FCGR3B CNV genotype frequencies in the controls). However, there are more profound differences between these two studies, and we believe it is the validity of the Haldersen et al.1 study that is in doubt.

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References

  1. Haldorsen K, Appel S, Le Hellard S, Bruland O, Brun JG, Omdal R et al. No association of primary Sjögren’s syndrome with Fcγ receptor gene variants. Genes Immun 2013; 14: 234–237.

    Article  CAS  Google Scholar 

  2. Breunis WB, van Mirre E, Geissler J, Laddach N, Wolbink G, van der Schoot E et al. Copy number variation at the FCGR locus includes FCGR3A, FCGR2C and FCGR3B but not FCGR2A and FCGR2B. Hum Mutat 2009; 30: E640–E650.

    Article  Google Scholar 

  3. McKinney C, Merriman TR . Meta-analysis confirms a role for deletion in FCGR3B in autoimmune phenotypes. Hum Mol Genet 2012; 21: 2370–2376.

    Article  CAS  Google Scholar 

  4. Mamtani M, Anaya JM, He W, Ahuja SK . Association of copy number variation in the FCGR3B gene with risk of autoimmune diseases. Genes Immun 2010; 11: 155–160.

    Article  CAS  Google Scholar 

  5. Nossent JC, Rischmueller M, Lester S . Low copy number of the Fc-γ receptor 3B gene FCGR3B is a risk factor for primary Sjogren’s syndrome. J Rheumatol 2012; 39: 2142–2147.

    Article  CAS  Google Scholar 

  6. Su K, Wu J, Edberg JC, McKenzie SE, Kimberly RP . Genomic organization of classical human low-affinity Fcgamma receptor genes. Genes Immun 2002; 3 (Suppl 1): S51–S56.

    Article  CAS  Google Scholar 

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Authors and Affiliations

  1. Rheumatology Department, The Queen Elizabeth Hospital, Woodville, South Australia, Australia

    S Lester & M Rischmueller

  2. Division of Medicine, Royal Darwin Hospital, Tiwi, Northern Territory, Australia

    J Nossent

  3. Discipline of Medicine, University of Adelaide, Adelaide, South Australia, Australia

    M Rischmueller

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  1. S Lester
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  2. J Nossent
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  3. M Rischmueller
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Correspondence to S Lester.

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Lester, S., Nossent, J. & Rischmueller, M. Comment on ‘No association of primary Sjögren’s syndrome with Fcγ receptor gene variants’. Genes Immun 14, 530–531 (2013). https://doi.org/10.1038/gene.2013.52

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