Lack of association between mannose-binding lectin gene polymorphisms and juvenile idiopathic arthritis in a Han population from the Hubei province of China

doi:10.1186/ar1953

Arthritis Res Ther. 2006; 8(4): R85.

Published online 2006 May 8. doi: 10.1186/ar1953

PMCID: PMC1779397

Lack of association between mannose-binding lectin gene polymorphisms and juvenile idiopathic arthritis in a Han population from the Hubei province of China

Min Kang,¹ Hong-Wei Wang,¹ Pei-Xuan Cheng,¹ Zun-Dong Yin,² Xiao-Ou Li,¹ Hong Shi,¹ and Xiu-Fen Hu¹

¹Department of Pediatrics, Tongji Hospital, Tongji Medical College, Hua Zhong University of Science and Technology, 1095 Jie Fang Avenue, Wuhan 430030, Hubei Province, China

²Chinese Center for Disease Control and Prevention, 27 Nan Wei Road, Beijing 100050, China

Corresponding author.

Min Kang: kang_m/at/hotmail.com; Hong-Wei Wang: hwwang/at/tjh.tjmu.edu.cn

Received January 1, 2006; Revisions requested February 8, 2006; Revised March 2, 2006; Accepted April 9, 2006.

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC.

Abstract

Many studies have reported that polymorphisms of the mannose-binding lectin (MBL) gene are associated with autoimmune disease. Here, we investigate the relationship between MBL gene polymorphisms and susceptibility to juvenile idiopathic arthritis (JIA) in a Han-nationality population from the Hubei province of China. PCR-restriction fragment length polymorphism was used to investigate polymorphisms of codons 54 and 57 in exon 1 of the MBL gene in 93 patients with JIA and 48 control children. Neither group showed codon 57 polymorphisms. There was no significant difference in the genotypic frequencies of codon 54 between patients with JIA and healthy controls (wild type, 71.0% versus 75.0%, respectively; heterozygous type, 25.8% versus 25.0%, respectively; and homozygous type, 3.2% versus 0.0%, respectively). In addition, no association was found between the subgroups of patients with JIA and control individuals. Our results provide no evidence for a relationship between MBL gene mutation and susceptibility to JIA.

Articles from Arthritis Research & Therapy are provided here courtesy of
BioMed Central