Journal
DIABETES
Volume 60, Issue 11, Pages 3081-3084Publisher
AMER DIABETES ASSOC
DOI: 10.2337/db11-0638
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Funding
- Juvenile Diabetes Research Foundation International (JDRF)
- Wellcome Trust [079895, G0000934, 068545/Z/02, 076113/C/04/Z]
- National Institute for Health Research Cambridge Biomedical Centre
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
- U.K. Medical Research Council
- Wellcome Trust/JDRF [061858]
- National Institute for Health Research of England
- National Institute of Allergy and Infectious Diseases
- National Human Genome Research Institute
- National Institute of Child Health and Human Development
- [U01 DK062418]
- British Heart Foundation [RG/08/014/24067] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0508-10275] Funding Source: researchfish
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OBJECTIVE-FUT2 encodes the alpha(1,2) fucosyltransferase that determines blood group secretor status. Homozygotes (A/A) for the common nonsense mutation rs601338A>G (W143X) are non-secretors and are unable to express histo-blood group antigens in secretions and on mucosal surfaces. This mutation has been reported to provide resistance to Norovims and susceptibility to Crohn's disease, and hence we aimed to determine if it also affects risk of type 1 diabetes. RESEARCH DESIGN AND METHODS-rs601338A>G was genotyped in 8,344 patients with type 1 diabetes, 10,008 control subjects, and 3,360 type 1 diabetic families. Logistic regression models were used to analyze the case-control collection, and conditional logistic regression was used to analyze the family collection. RESULTS-The nonsecretor A/A genotype of rs601338A>G was found to confer susceptibility to type 1 diabetes in both the case-control and family collections (odds ratio for AA 1.29 [95% CI 1.20-1.37] and relative risk for AA 1.22 [95% CI = 1.12-1.32]; combined P = 4.3 x 10(-18)), based on a recessive effects model. CONCLUSIONS-Our findings linking FUT2 and type 1 diabetes highlight the intriguing relationship between host resistance to infections and susceptibility to autoimmune disease. Diabetes 60:3081-3084, 2011
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