Related resources
Full-text held externally
- DOI: 10.1186/ar3139
- PMID: 20854658
- UKPMCID: 20854658
Search for item elsewhere
University researcher(s)
Academic department(s)
Overlapping genetic susceptibility variants between three autoimmune disorders: rheumatoid arthritis, type 1 diabetes and coeliac disease.
Eyre, Steve; Hinks, Anne; Bowes, John; Flynn, Edward; Martin, Paul; Wilson, Anthony G; Morgan, Ann W; Emery, Paul; Steer, Sophia; Hocking, Lynn J; Reid, David M; Harrison, Pille; Wordsworth, Paul; Yorkshire_Early_Arthritis_(YEAR)_Consortium, Yorkshire Early Arthritis Year; Biologics_in_RA_Control_(BIRAC)_Consortium, Biologics In Ra Control Birac; Thomson, Wendy; Worthington, Jane; Barton, Anne
Arthritis research & therapy. 2010;12(5):R175.
Access to files
Full-text and supplementary files are not available from Manchester eScholar. Full-text is available externally using the following links:
Full-text held externally
- DOI: 10.1186/ar3139
- PMID: 20854658
- UKPMCID: 20854658
Abstract
ABSTRACT: INTRODUCTION: Genome wide association studies, replicated by numerous well powered validation studies, have revealed a large number of loci likely to play a role in susceptibility to many multifactorial diseases. It is now well established that some of these loci are shared between diseases with similar aetiology. For example, a number of autoimmune diseases have been associated with variants in the PTPN22, TNFAIP3 and CTLA4 genes. Here we have attempted to define overlapping genetic variants between rheumatoid arthritis (RA), type 1 diabetes (T1D) and coeliac disease (CeD). METHODS: We selected 8 SNPs previously identified as being associated with CeD and 6 T1D-associated SNPs for validation in a sample of 3,962 RA patients and 3,531 controls. Genotyping was performed using the Sequenom MassArray platform and comparison of genotype and allele frequencies between cases and controls was undertaken. A trend test P-value <0.004 was regarded as significant. RESULTS: We found statistically significant evidence for association of the TAGAP locus with RA (P = 5.0 x 10-4). A marker at one other locus, C1QTNF6, previously associated with T1D, showed nominal association with RA in the current study but did not remain statistically significant at the corrected threshold. CONCLUSIONS: In exploring the overlap between T1D, CeD and RA, there is strong evidence that variation within the TAGAP gene is associated with all three autoimmune diseases. Interestingly a number of loci appear to be specific to one of the three diseases currently studied suggesting that they may play a role in determining the particular autoimmune phenotype at presentation.
Bibliographic metadata
- Eyre, Steve
- Hinks, Anne
- Bowes, John
- Flynn, Edward
- Martin, Paul
- Wilson, Anthony G
- Morgan, Ann W
- Emery, Paul
- Steer, Sophia
- Hocking, Lynn J
- Reid, David M
- Harrison, Pille
- Wordsworth, Paul
- Yorkshire_Early_Arthritis_(YEAR)_Consortium, Yorkshire Early Arthritis Year
- Biologics_in_RA_Control_(BIRAC)_Consortium, Biologics In Ra Control Birac
- Thomson, Wendy
- Worthington, Jane
- Barton, Anne