Research Papers:
Association of IL-1A and IL-1B polymorphisms with ankylosing spondylitis among the Chinese Han population: a case–control study
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Abstract
Lei Li1,2,*, Baolan Shi1,4,*, Wenkai Zheng1,2, Wenhua Xing2, Yan Zhao2, Feng Li2, Daqi Xin2, Tianbo Jin3, Yong Zhu2, Xuejun Yang2
1Inner Mongolia Medical University, Hohhot 010020, China
2The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010030, China
3Key Laboratory of Resource Biology and Biotechnology in Western China (Northwest University), Ministry of Education, Xi’an, Shaanxi 710069, China
4Inner Mongolia Medical University, Chifeng Clinical Medical College, ChiFeng, 024000, China
*Joint first authors
Correspondence to:
Yong Zhu, email: [email protected]
Xuejun Yang, email: [email protected]
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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