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Ann Rheum Dis. 2019 Jan;78(1):66-73. doi: 10.1136/annrheumdis-2018-213779. Epub 2018 Oct 19.

HLA class I and II alleles in susceptibility to ankylosing spondylitis.

Author information

1
Division of Rheumatology and Clinical Immunogenetics, McGovern Medical School at The University of Texas Health Science Center, Houston, Texas, USA john.d.reveille@uth.tmc.edu.
2
Division of Rheumatology and Clinical Immunogenetics, McGovern Medical School at The University of Texas Health Science Center, Houston, Texas, USA.
3
Division of Clinical and Translational Sciences, McGovern Medical School at The University of Texas Health Science Center, Houston, Texas, USA.
4
Department of Radiology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
5
Division of Rheumatology, Gansu College of Traditional Chinese Medicine, Gansu, China.
6
Division of Rheumatology, The University of California, San Francisco, California, USA.
7
Huashan Hospital, Fudan University, Shanghai, China.
8
Division of Rheumatology, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, Maryland, USA.
9
Division of Rheumatology, Shanghai Guanghua Hospital, Shanghai, China.
10
Institute of Health and Biomedical Innovation, Queensland University of Technology, Translational Research Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia.

Abstract

OBJECTIVE:

To examine associations of HLA class I and class II alleles with ankylosing spondylitis (AS) in three cohorts of patients of European, Asian and African ancestry.

METHODS:

HLA-A, HLA-B, HLA-C, HLA-DRB1, HLA-DQB1 and HLA-DPB1 alleles were genotyped in 1948 unrelated white and 67 African-American patients with AS from the Prospective Study of Outcomes in Ankylosing Spondylitis cohort, the North American Spondylitis Consortium and Australo-Anglo-American Spondyloarthritis Consortium, 990 white and 245 African-American Controls and HLA-B alleles in 442 Han Chinese patients with AS and 346 controls from Shanghai and Gansu, China. In addition to the case:control analyses, HLA-B*27-negative patients with AS were analysed separately, and logistic regression and 'relative predispositional effects' (RPE) analyses were carried out to control for the major effect of HLA-B*27 on disease susceptibility.

RESULTS:

Although numerous associations were seen between HLA alleles and AS in whites, among HLA-B*27-negative patients with AS , positive associations were seen with HLA-A*29, B*38, B*49, B*52, DRB1*11 and DPB1*03:01 and negative associations with HLA-B*07, HLA-B*57, HLA-DRB1*15:01, HLA-DQB1*02:01 and HLA -DQB1*06:02. Additional associations with HLA-B*14 and B*40 (B60) were observed via RPE analysis, which excludes the HLA-B*27 alleles. The increased frequency of HLA-B*40:01 and decreased frequency of HLA-B*07 was also seen in Han Chinese and African-Americans with AS. HLA-B*08 was decreased in whites with acute anterior uveitis.

CONCLUSIONS:

These data, analysing the largest number of patients with AS examined to date in three ethnic groups, confirm that other HLA class I and II alleles other than HLA-B*27 to be operative in AS predisposition.

KEYWORDS:

African-American; Chinese; HLA; disease susceptibility; ethnicity; spondylitis; uveitis

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