The Open Rheumatology Journal




ISSN: 1874-3129 ― Volume 14, 2020

Profiling of HLA-B Alleles for Association Studies with Ankylosing Spondylitis in the Chinese Population



Lin Yi1, 2, §, Jiucun Wang3, 5, §, Xinjian Guo1, Maribel G. Espitia1, Enuo Chen1, Shervin Assassi1, Li Jin3, Hejian Zou4, 5, * , John D. Reveille 1, Xiaodong Zhou1, §
1 Division of Rheumatology and Clinical Immunogenetics, University of Texas Medical School at Houston, USA
2 Gansu College of Traditional Chinese Medicine, Lanzhou, Gansu, China
3 State Key Laboratory of Genetic Engineering and Ministry of Education Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, China
4 Huashan Hospital, Fudan University, China
5 Institute of Rheumatology, Immunology, and Allergy, Fudan University, China

Abstract

Human leucocyte antigen (HLA) B*27 is a susceptibility allele to ankylosing spondylitis (AS). However, major AS-associated subtypes of HLA-B*27 and other HLA-B alleles vary in different ethnic populations. Herein, we examined HLA-B alleles in a total of 360 AS patients and 350 controls of Chinese Han ancestry. The HLA-B genotyping was performed with sequence-based typing (SBT) method. Six HLA-B*27 subtypes B*27:04, B*27:05, B*27:07, B*27:08, B*27:10 and B*27:15 were observed in the cohorts. HLA-B*27:04:01 and -B*27:05:02 appeared significantly increased in AS patients, which indicated as two major susceptibility alleles to AS. Homozygous B*27 was observed only in AS patients. There are 30 HLA-B alleles identified in the studies. HLA-B*15, especially B*15:01:01:01, appeared as the major allele type in the Chinese controls. Some common HLA-B alleles such as HLA-B*15, B*13, B*46 and B*51 were significantly reduced in Chinese AS patients. In conclusion, the studies profiled the HLA-B alleles, and identified major susceptibility subtypes of B27 to AS in Han Chinese population

Keywords: Ankylosing spondylitis (AS), HLA-B27, Chinese Han..

Article Information


Identifiers and Pagination:

Year: 2013
Volume: 7
First Page: 51
Last Page: 54
Publisher Id: TORJ-7-51
DOI: 10.2174/1874312920130628001

Article History:

Received Date: 22/5/2013
Revision Received Date: 19/6/2013
Acceptance Date: 24/6/2013
Electronic publication date: 19 /8/2013
Collection year: 2013

© Yi et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.


* Address correspondence to these authors at the Division of Rheumatology and Clinical Immunogenetics, University of Texas Medical School at Houston, 6431 Fannin Street, Room 5.270 Houston, Texas 77030, USA; Tel: 713-500-6900; Fax: 713-500-0580; E-mail: xiaodong.zhou@uth.tmc.edu and Huashan Hospital, Fudan University, China; Tel: +86-21-52888808; Fax: +86-21-62489191; E-mail: hejianzou@gmail.com§ Authors equally contributed.



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