A general autoimmunity gene (PTPN22) is not associated with inflammatory bowel disease in a British population

Prescott, N J, Fisher, S A, Onnie, C, Pattni, R, Steer, S, Sanderson, J, Forbes, A, Lewis, C M and Mathew, C G (2005) A general autoimmunity gene (PTPN22) is not associated with inflammatory bowel disease in a British population. Tissue Antigens, 66 (4). pp. 318-20. ISSN 0001-2815

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Abstract

A single-nucleotide polymorphism (C1858T) causing an amino acid substitution (R620W) in the lymphoid protein tyrosine phosphatase gene PTPN22 has been implicated in type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, Graves' disease, juvenile idiopathic arthritis and Hashimoto's thyroiditis, thus revealing a general role for this gene in autoimmune disease. We investigated the association of the C1858T variant in an additional autoimmune disease population by performing a case-control study of 514 British individuals with inflammatory bowel disease (IBD) [294 with Crohn's disease (CD) and 220 with ulcerative colitis (UC)] and 374 normal controls. No significant differences in genotype or allele frequencies were observed between IBD, CD or UC and controls, indicating that PTPN22 does not influence risk of IBD.

Item Type: Article
Uncontrolled Keywords: amino acid substitution,autoimmune diseases,case-control studies,colitis, ulcerative,crohn disease,genetic predisposition to disease,genotype,great britain,polymorphism, single nucleotide,protein tyrosine phosphatase, non-receptor type 1,protein tyrosine phosphatase, non-receptor type 22,protein tyrosine phosphatases,risk factors
Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
University of East Anglia > Faculty of Medicine and Health Sciences > Research Groups > Gastroenterology and Gut Biology
University of East Anglia > Faculty of Medicine and Health Sciences > Research Groups > Nutrition
Depositing User: Pure Connector
Date Deposited: 06 Aug 2014 11:54
Last Modified: 28 Aug 2018 11:31
URI: https://ueaeprints.uea.ac.uk/id/eprint/49640
DOI: 10.1111/j.1399-0039.2005.00494.x

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