Non-B27 MHC associations of ankylosing spondylitis

Sims, A. M.; Barnardo, Martin; Herzberg, I.; Bradbury, L.; Calin, Andrei; Wordsworth, B P; Darke, C.; Brown, Matthew A.

doi:10.1038/sj.gene.6364362

Cited by 44 publications

(27 citation statements)

References 63 publications

(31 reference statements)

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“…This finding has been supported by the results obtained in different ethnic groups (Brown, et al, 1998a;Jaakkola, et al, 2006;Kchir, et al, 2010;Mahfoudh, et al, 2011;Ploski, et al, 1995;SaidNahal, et al, 2002;Sims, A M, et al, 2007). HLA-DRB1 was found to have a strong association with AS.…”

Section: Introductionsupporting

confidence: 80%

“…HLA-DRB1*08 had been already reported in juvenile-AS B27-positive individuals, in Norwegian population (Ploski, et al, 1995). Two haplotypes were identified in a British case-control study: B*27positive /DRB1*07positive and B*27negative /DRB1*03positive (Sims, A M, et al, 2007). The frequency of HLA-DRB1*15 was found to be increased, in Tunisian AS patients, but this allele was in LD with B27 (Mahfoudh, et al, 2011).…”

Section: Introductionmentioning

confidence: 90%

“…HLA-DRB1 was found to have a strong association with AS. In British patients the level of this association was increased in DR1 homozygotes, a fact that may suggest a B27-independent association, excluding a possible LD effect (Brown, et al, 1998a;Sims, A M, et al, 2007). On the other hand, in French families the association between DR1 and AS seems to be a consequence of LD with HLA-B27 (SaidNahal, et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Genetics in Ankylosing Spondylitis – Beyond HLA-B*27

Bettencourt¹,

Foroni²,

Couto³

et al. 2012

Clinical and Molecular Advances in Ankylosing Spondylitis

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Section: Introductionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Genetics in Ankylosing Spondylitis – Beyond HLA-B*27

Bettencourt¹,

Foroni²,

Couto³

et al. 2012

Clinical and Molecular Advances in Ankylosing Spondylitis

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“…Previously, HLA-DRB1*01 has been associated with periodontal pathogens in Finnish coronary artery disease patients [18] and with juvenile idiopathic arthritis in Hungarian patients [19]. HLA-B*27 and HLA-B*35, frequently carried with HLA-DRB1*01 haplotypes, have been associated with infectious or postinfectious complications in reactive arthritis [20], chronic herpes simplex virus [21], HIV [13], Chlamydia pneumoniae [22], and Sin Nombre virus infections [23].…”

Section: Discussionmentioning

confidence: 99%

HLA-DRB1*01 allele and low plasma immunoglobulin G1 concentration may predispose to herpes-associated recurrent lymphocytic meningitis

et al. 2010

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“…12 A study of non-B27 MHC associations of AS using B27-matched haplotypes in cases and controls has shown that HLA-DRB1 is associated with AS irrespective of whether the haplotype contained HLA-B27. 69 This may contribute to disease by causing aberrant presentation to or selection of CD4+ lymphocytes.…”

Section: Other Mhc Genesmentioning

confidence: 99%

The genomics and genetics of ankylosing spondylitis

Kenna¹,

Davidson²,

Thomas³

2011

AGG

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Abstract:The spondyloarthropathies are a group of arthritides which specifically target the spine and pelvis with ankylosing spondylitis (AS) being the most prevalent and debilitating of these conditions. Unique to AS is the progression to excessive uncontrolled bone formation following an initial inflammatory phase that can result in joint fusion and significant disability. Spondyloarthritis is estimated to affect 1%-2% of the population, twice as many as rheumatoid arthritis and thus constitutes a significant health problem. Currently AS pathogenesis is very poorly understood but recent large-scale genetics and gene expression profiling studies have identified some of the underlying mechanisms and pathways contributing to the disease. Genome-wide association studies have identified a number of candidate genes associated with AS sharing the same pathways which are now being targeted for therapeutic intervention. However, although such approaches can identify genes contributing to the disease process and are very informative as to disease aetiopathogenesis, they cannot profile the actual changes in gene/cell activity at any point in the disease process or possibly more importantly at specific sites. Such information is generated using expression profiling. A number of expression profiling studies have been undertaken in AS, looking at both circulating cells and tissues from affected joints. Although some common genes/pathways have been identified, overall the results to date have been somewhat disappointing due to differences in experimental design and tissue source as well as the low power of the studies. More recent better powered studies have shown some potential in developing gene expression profiling as a diagnostic tool in AS. True future success will rely on larger genetic and genomic studies and the combination of these datasets in eQTL studies requiring significant collaborative efforts. Such larger-scale approaches will also generate sufficient power to target specific disease stages and sites.

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Non-B27 MHC associations of ankylosing spondylitis

Cited by 44 publications

References 63 publications

Genetics in Ankylosing Spondylitis – Beyond HLA-B*27

Genetics in Ankylosing Spondylitis – Beyond HLA-B*27

HLA-DRB1*01 allele and low plasma immunoglobulin G1 concentration may predispose to herpes-associated recurrent lymphocytic meningitis

The genomics and genetics of ankylosing spondylitis

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