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The functional polymorphism 844 A>G in FcαRI (CD89) does not contribute to systemic sclerosis or rheumatoid arthritis susceptibility

Broen, JCA (author)
Coenen, MJH (author)
Rueda, B (author)
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Witte, T (author)
Padyukov, L (author)
Karolinska Institutet
Klareskog, L (author)
Karolinska Institutet
Hesselstrand, R (author)
Wuttge, DM (author)
Simeon, C (author)
Ortego-Centeno, N (author)
Gonzalez-Gay, MA (author)
Pros, A (author)
Hunzelman, N (author)
Riemekasten, G (author)
Kreuter, A (author)
Vonk, M (author)
Scorza, R (author)
Beretta, L (author)
Airo, P (author)
van Riel, PLCM (author)
Kimberly, R (author)
Martin, J (author)
Edberg, J (author)
Radstake, TRDJ (author)
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 (creator_code:org_t)
2010-12-15
2011
English.
In: The Journal of rheumatology. - : The Journal of Rheumatology. - 0315-162X .- 1499-2752. ; 38:3, s. 446-449
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • To investigate the role of the FcαRI 844 A>G functional polymorphism in the genetic predisposition to rheumatoid arthritis (RA) and systemic sclerosis (SSc) susceptibility.Methods.The study population was composed of 1401 patients with SSc, 642 patients with RA, and 1317 healthy controls. The FcαRI (CD89) single-nucleotide polymorphism rs16986050 was genotyped by pyrosequencing.Results.We observed no significant deviation of the genotype and allele frequencies in RA and SSc compared to controls. A metaanalysis and a recessive and dominant model yielded similar negative results.Conclusion.Our data show that the FcαRI 844 A>G polymorphism is not associated with SSc or RA susceptibility.

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