Association of IL-1A and IL-1B polymorphisms with ankylosing spondylitis among the Chinese Han population: a case–control study

2017 
// Lei Li 1, 2, * , Baolan Shi 1, 4, * , Wenkai Zheng 1, 2 , Wenhua Xing 2 , Yan Zhao 2 , Feng Li 2 , Daqi Xin 2 , Tianbo Jin 3 , Yong Zhu 2 , Xuejun Yang 2 1 Inner Mongolia Medical University, Hohhot 010020, China 2 The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010030, China 3 Key Laboratory of Resource Biology and Biotechnology in Western China (Northwest University), Ministry of Education, Xi’an, Shaanxi 710069, China 4 Inner Mongolia Medical University, Chifeng Clinical Medical College, ChiFeng, 024000, China * Joint first authors Correspondence to: Yong Zhu, email: 1036227632@qq.com Xuejun Yang, email: yangxuejun2004@126.com Keywords: ankylosing spondylitis (AS), single nucleotide polymorphism (SNP), IL-1A, IL-1B, case-control study Received: September 24, 2016      Accepted: February 21, 2017      Published: March 08, 2017 ABSTRACT Ankylosing spondylitis (AS) is a complex and chronic inflammatory disease with a high heritage. Previous study has shown that IL-1A and IL-1B involved in inflammatory reaction. But little is known about single nucleotide polymorphisms (SNPs) of IL-1A and IL-1B associated with AS. We conducted a case-control study among 267 AS cases and 297 healthy controls from China. In the genetic model analysis, we found the “T” genotype of rs3783550 was associated with decreased AS risk in the dominant model ( p = 0.044) and log-additive model ( p = 0.023); the “C” genotype of rs3783546 was significantly associated with decreased AS risk based in the dominant model ( p = 0.044) and log-additive model ( p = 0.023). Additionally, the minor allele “A” of rs2853550 may also reduce the risk of AS in dominant ( p = 0.025) and log-additive model ( p = 0.024). Our results suggested that the polymorphisms of IL-1A and IL-1B are associated with the AS susceptibility in the Chinese Han population. Further studies are needed to characterize the functional sequences that cause AS.
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