The PRL -1149 G/T polymorphism and rheumatoid arthritis susceptibility

Yvonne C. Lee, Soumya Raychaudhuri, Jing Cui, Immaculata De Vivo, Bo Ding, Lars Alfredsson, Leonid Padyukov, Karen H. Costenbader, Mark Seielstad, Robert R. Graham, Lars Klareskog, Peter K. Gregersen, Robert M. Plenge, Elizabeth W. Karlson

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

Objective. Previous studies have demonstrated that the PRL -1149 T (minor) allele decreases prolactin expression and may be associated with autoimmune disease. The aim of this study was to determine the role of the PRL -1149 G/T polymorphism (rs1341239) in rheumatoid arthritis (RA) susceptibility. Methods. We examined the association between PRL -1149 G/T and RA risk in 4 separate study populations, consisting of a total of 3,405 RA cases and 4,111 controls of self-reported white European ancestry. Samples were genotyped using 1 of 3 genotyping platforms, and strict quality control metrics were applied. We tested for association using a 2-tailed Cochran-Mantel-Haenszel additive, fixed-effects model. Results. In the individual populations, odds ratios (ORs) for an association between PRL -1149 T and RA risk ranged from 0.80 to 0.97. In a joint meta-analysis across all 4 populations, the OR for an association between PRL -1149 T and RA risk was 0.90 (95% confidence interval 0.84-0.96, P = 0.001). Conclusion. Our findings indicate a possible association between the PRL -1149 T allele and decreased RA risk. The effect size is small but similar to ORs for other genetic polymorphisms associated with complex traits, including RA.

Original languageEnglish (US)
Pages (from-to)1250-1254
Number of pages5
JournalArthritis and rheumatism
Volume60
Issue number5
DOIs
StatePublished - May 2009

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Immunology and Allergy
  • Rheumatology
  • Immunology

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