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http://purl.uniprot.org/citations/15089899http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15089899http://www.w3.org/2000/01/rdf-schema#comment"

Objective

The aim of this study was to investigate the association of MHC genes in the development of celiac disease (CD) and its diverse clinical forms in a Saharawi population.

Methods

One hundred and twenty-five CD patients and 98 healthy controls were selected from the Saharawi refugee camps in Tindouf. All were investigated for the presence of antitransglutaminase 2 antibodies. Patients were divided into two groups according to their clinical manifestations: 70 typical and 55 atypical. Patients and controls were typed for HLA-B, DRB1, DQB1, and DQA1, and for MICA transmembrane polymorphism.

Results

The frequency of HLA-DQ2 in Saharawi controls was notably increased compared with other populations. No differences in the distribution of DQ2 in either group of patients were found. However, the haplotype B8/DR3/DQ2 was notably overrepresented in atypical patients compared to typical ones (pc= 0.001). The MICA-A5.1 allele was increased in atypical CD patients compared to those with typical forms (pc= 0.0006). Finally, we found that the increased frequency of MICA-A5.1 in the atypical group was independent of the linkage disequilibrium with B8/DR3/DQ2 haplotype (p= 0.02).

Conclusions

The elevated prevalence of CD in Saharawi seems to be related to the high frequency of HLA-DQ2 in this population. However, the development of atypical or typical forms of the disease may be due to a gene or genes located in the class I side of the haplotype B8/DR3/DQ2, especially MICA. This appears not to be implicated in the susceptibility to CD but may play an important role in the development of the different forms of the disease."xsd:string
http://purl.uniprot.org/citations/15089899http://purl.org/dc/terms/identifier"doi:10.1111/j.1572-0241.2004.04134.x"xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/author"Fernandez E."xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/author"Gonzalez S."xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/author"Fuentes D."xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/author"Moreno M."xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/author"Lopez-Larrea C."xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/author"Lopez-Vazquez A."xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/author"Martinez-Borra J."xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/author"Rodrigo L."xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/name"Am J Gastroenterol"xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/pages"662-667"xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/title"MHC class I region plays a role in the development of diverse clinical forms of celiac disease in a Saharawi population."xsd:string
http://purl.uniprot.org/citations/15089899http://purl.uniprot.org/core/volume"99"xsd:string
http://purl.uniprot.org/citations/15089899http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15089899
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