ArticleAnnals of the rheumatic diseases2002
The role of HLA genes in familial spondyloarthropathy: a comprehensive study of 70 multiplex families.
Article in Annals of the rheumatic diseases, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 55 citations in OpenAlex.
- Role of HLA class I and II alleles in susceptibility to ankylosing spondylitis in Chinese Han.Journal of clinical laboratory analysis · 2023Article
- HLA class I and II alleles in susceptibility to ankylosing spondylitis.Annals of the rheumatic diseases · 2019Article
- Genetics and the Causes of Ankylosing Spondylitis.Rheumatic diseases clinics of North America · 2017Review
- Association of human leukocyte A, B, and DR antigens in Colombian patients with diagnosis of spondyloarthritis.Clinical rheumatology · 2017Article
- HLA-DRB1 the notorious gene in the mosaic of autoimmunity.Immunologic research · 2017Article
- Revisiting MHC genes in spondyloarthritis.Current rheumatology reports · 2015Review
- An update on the contribution of the MHC to AS susceptibility.Clinical rheumatology · 2014Review
- HLA-B, DR and DQ antigens polymorphism in Tunisian patients with ankylosing spondylitis (a case-control study).Rheumatology international · 2010Article
- Non-B27 MHC associations of ankylosing spondylitis.Genes and immunity · 2007Article
- Article
- The genetic basis of spondyloarthritis.Current rheumatology reports · 2004Review
- HLA-DR4 and the spondyloarthropathies.Annals of the rheumatic diseases · 2002Article
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo investigate whether HLA alleles, other than HLA-B27, influence predisposition to spondyloarthropathy (SpA) in multiplex families.
methodsSeventy French families with at least two affected SpA members were recruited. Patients, and their first degree relatives were typed for HLA-A, B, C, and DR, and extended HLA haplotypes were determined. The distribution of HLA-A, C, and DR alleles carried on HLA-B27+ haplotypes in SpA families was compared with the distribution of these alleles among HLA-B27+ haplotypes in the French general population. Contribution to SpA susceptibility of HLA-A, B, C, and DR alleles, other than HLA-B27, was tested by transmission disequilibrium test. The contribution of HLA alleles to specific presentation features of SpA was examined.
resultsFrequencies of HLA-A, C, and DR alleles carried on HLA-B27+ haplotypes from SpA families were comparable with those seen in the French population, except for DR13 which was overrepresented among patients (pcorr<0.001). Most interestingly, the HLA-DR4 allele was transmitted in excess to patients with SpA, independently of linkage to HLA-B27 (pcorr=0.05), and in a direction opposite to that for HLA-B27+ unaffected siblings (pcorr=0.01). Finally, the distribution of HLA alleles was not related to the presentation feature of SpA.
conclusionHLA predisposition to familial SpA appears not to be limited to HLA-B27, but some HLA-DR alleles also have a significant influence. In particular, HLA-DR4 contributes significantly to a genetic predisposition to SpA, which may have implications in our understanding of SpA pathogenesis.
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