<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Kim, Tae-Hwan</style></author><author><style face="normal" font="default" size="100%">Stone, Millicent A</style></author><author><style face="normal" font="default" size="100%">Rahman, Proton</style></author><author><style face="normal" font="default" size="100%">Yoo, Dae-Hyun</style></author><author><style face="normal" font="default" size="100%">Park, Yong-Wook</style></author><author><style face="normal" font="default" size="100%">Payne, Ursula</style></author><author><style face="normal" font="default" size="100%">Hallett, Dave</style></author><author><style face="normal" font="default" size="100%">Inman, Robert D</style></author></authors><secondary-authors></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Interleukin 1 and nuclear factor-kappaB polymorphisms in ankylosing spondylitis in Canada and Korea.</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of Rheumatology</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2005</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2005-10-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">1907-1910</style></pages><volume><style face="normal" font="default" size="100%">32</style></volume><issue><style face="normal" font="default" size="100%">10</style></issue><abstract><style  face="normal" font="default" size="100%">OBJECTIVE: The interleukin 1alpha and 1beta (IL-1alpha, IL-1beta) are potent mediators of inflammation and immunity. IL-1 receptor antagonist (IL-1Ra) is a protein that binds to IL-1 receptors and competitively inhibits the binding of IL-1alpha and IL-1beta. There are reports of IL-1 complex gene polymorphisms in ankylosing spondylitis (AS), but the results have been inconsistent. NFKB1 encodes the genes for the p50 and p101 nuclear factor-kappaB (NF-kappaB) isoforms, which are recognized as critical to inflammatory disease. To date there have been no reports examining an association between NFKB1 and AS. We investigated polymorphisms of IL-1 complex and NF-kappaB1 with 2 genetically and geographically different populations. METHODS: Subjects with AS satisfied modified New York criteria for AS. Healthy controls were recruited at each respective site. Subjects with AS were genotyped for the following: IL-1alpha-889 single nucleotide polymorphism (SNP); IL-1beta +3953 SNP; IL-1Ra (86 base pair variable number tandem repeat within intron 2); and NFKB1 (-94 insertion/deletion polymorphism). RESULTS: In total, 205 subjects with AS and 200 controls from Seoul, Korea, and 68 subjects with AS and 164 controls from Toronto, Canada, were genotyped for the IL-1alpha and IL-1beta polymorphisms and 115 controls for the IL-1Ra and NF-kappaB polymorphisms. There were no differences of IL-1alpha, IL-1beta, IL-1Ra, and NF-kappaB polymorphisms between AS patients and controls in these populations. CONCLUSION: Our analysis of these SNP in the IL-1 complex and NF-kappaB genes does not support a major role for either in AS susceptibility in the Seoul and Toronto populations.</style></abstract></record></records></xml>