The effect of HLA‐DR genes on susceptibility to and severity of ankylosing spondylitis

Brown, Matthew A.; Kennedy, L G; Darke, C.; Gibson, Karen J.; Pile, K; Shatford, J; Taylor, Andrew; Calin, Andrei; Wordsworth, B P

doi:10.1002/1529-0131(199803)41:3<460::aid-art12>3.3.co;2-o

Cited by 65 publications

(37 citation statements)

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“…Previous studies had confirmed that the genetic factors play an important role in the pathogenesis of AS [4]. The human leukocyte antigen (HLA)-B27 is the first genetic factor identified in this disease, and it confers the greatest susceptibility to AS (20-30 %) [5,6]. However, HLA-B27 cannot explain all patients with AS, as only 5 % of HLA-B27-positive individuals ultimately develop to AS [7], indicating that other non-HLA-B27 susceptibility genes could contribute to AS susceptibility.…”

Section: Introductionmentioning

confidence: 97%

The associations between PD-1, CTLA-4 gene polymorphisms and susceptibility to ankylosing spondylitis: a meta-analysis and systemic review

Chen¹,

Y²,

Deng³

et al. 2015

Rheumatol Int

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Previous surveys had evaluated the effects of the PD-1, CTLA-4 gene polymorphisms on susceptibility to ankylosing spondylitis (AS), but the results remained controversial. To briefly examine these consequences, a comprehensive meta-analysis was conducted to estimate the relationships between PD-1 rs11568821, rs2227982, rs2227981, CTLA-4 +49 A/G and -318 C/T polymorphisms and AS risk. The available articles dated to December 2014 were searched in the PUBMED, MEDLINE and EMBASE databases. The data of the genotypes and/or alleles for the PD-1 rs11568821, rs2227982, rs2227981, CTLA-4 +49 A/G and -318 C/T polymorphisms in the AS and control subjects were extracted, and statistical analysis was conducted by STATA 11.2 software. Summary odds ratios (ORs) with their 95 % confidence intervals (95 % CIs) were calculated to determine the strength of associations with fixed-effects or random-effects models. A total of eight published studies were finally involved in this meta-analysis. Meta-analysis of PD-1 rs2227982 polymorphism under the T allele versus C allele (OR 1.744, 95 % CI 1.477-2.059, P < 0.0001), TT+TC versus CC (OR 2.292, 95 % CI 1.654-3.175, P < 0.0001), TT versus CC (OR 1.883, 95 % CI 1.299-2.729, P = 0.001) revealed a significant association with AS. Our meta-analysis demonstrated that the rs2227982 polymorphism in the PD-1 gene might contribute to AS susceptibility. However, further studies with large sample sizes and among different ethnicity populations should be required to confirm this association.

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Section: Introductionmentioning

confidence: 97%

The associations between PD-1, CTLA-4 gene polymorphisms and susceptibility to ankylosing spondylitis: a meta-analysis and systemic review

Chen¹,

Y²,

Deng³

et al. 2015

Rheumatol Int

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“…Consequently, it can be difficult to distinguish effects of the TNF gene locus from MHC gene effects. In this respect, the well-known association of ReA and of AS with HLA-B27 and of AS with HLA-DR1, as recently reported [79], may be of interest. In a Dutch study [80], HLA DR1 is associated with a low TNF␣ secretor haplotype which is also associated with the common TNF1 allele of the -308 TNF␣ promotor polymorphism, whereas DR3 is associated with higher secretion of TNF␣ and the uncommon TNF2 allele.…”

Section: The Strength and Human Leukocyte Antigen Relation Of Cellulamentioning

confidence: 76%

Cytokines and the immunopathology of the spondyloarthropathies

Braun

Sieper

1999

Curr Rheumatol Rep

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In contrast to rheumatoid arthritis (RA), the triggering antigens are known in reactive arthritis (ReA) and Lyme arthritis. Thus, in these arthritides the antigen-specific T-cell response can be investigated in much detail and lessons possibly learned for other spondyloarthropathies (SpA) such as ankylosing spondylitis (AS) where T cells may well also play an important role in the pathogenesis. This article focusses on the immunopathology of the SpA, ReA, and AS with special reference to T cells and cytokines.

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“…The entire effect of the major histocompatibility complex (MHC), however, is approximately 50%. Other MHC genes also have been implicated in AS in addition to B27, including HLA-DRB1 [26,27], MHC class I chain-related protein A [28], TNF-α [29,30], heat shock protein 70 [31], transporter associated with antigen processing-1 [32], and latent membrane protein-2 [33]. Psoriasis per se has been associated with HLA-B13, B37, and B57, which are linked to HLA-Cw6 (C*0602) [34].…”

Section: Other Major Histocompatibility Genesmentioning

confidence: 99%

The genetic basis of spondyloarthritis

Reveille

2004

Curr Rheumatol Rep

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Spondyloarthritis tends to cluster in families and, to a great extent, is associated with human leukocyte antigen (HLA) B27. In fact, the population frequency of spondyloarthritis in most groups is proportional to that of HLA-B27. But the frequency of HLA-B27 in the population-at-large far exceeds that of spondyloarthritis, suggesting other genetic factors also are operative. Other major histocompatibility complex genes have been implicated, especially HLA-DR, though linkage to HLA-B27 confounds the analysis of this in many studies. Genome-wide scans have implicated regions on chromosomes 2q, 6p, 6q, 10q, 11q, 16q, 17q, and 19q in ankylosing spondylitis, on 4, 6p, and 17q in psoriasis, and on 7q and 16q in inflammatory bowel disease. The search for non-major histocompatibility complex candidate genes has been complicated by inadequate power, because of the small effect they exert on overall disease susceptibility, although recent studies are revealing promising candidates that must be confirmed by other groups.

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The effect of HLA‐DR genes on susceptibility to and severity of ankylosing spondylitis

Cited by 65 publications

References 0 publications

The associations between PD-1, CTLA-4 gene polymorphisms and susceptibility to ankylosing spondylitis: a meta-analysis and systemic review

The associations between PD-1, CTLA-4 gene polymorphisms and susceptibility to ankylosing spondylitis: a meta-analysis and systemic review

Cytokines and the immunopathology of the spondyloarthropathies

The genetic basis of spondyloarthritis

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