Localization of PSORS1 to a haplotype block harboring HLA-C and distinct from corneodesmosin and HCR
Identifieur interne : 000216 ( Main/Exploration ); précédent : 000215; suivant : 000217Localization of PSORS1 to a haplotype block harboring HLA-C and distinct from corneodesmosin and HCR
Auteurs : Cynthia Helms [États-Unis] ; Nancy L. Saccone [États-Unis] ; Li Cao [États-Unis] ; Jil A. Wright. Daw [États-Unis] ; Kai Cao [États-Unis] ; Tony M. Hsu [États-Unis] ; Patricia Taillon-Miller [États-Unis] ; Shenghui Duan [États-Unis] ; Derek Gordon [États-Unis] ; Brandon Pierce [États-Unis] ; Jurg Ott [États-Unis] ; John Rice [États-Unis] ; Marcelo A. Fernandez-Vina [États-Unis] ; Pui-Yan Kwok [États-Unis] ; Alan Menter [États-Unis] ; Anne M. Bowcock [États-Unis]Source :
- Human Genetics [ 0340-6717 ] ; 2005-12-01.
Abstract
Abstract: Psoriasis is a complex inflammatory disease of the skin affecting 1–2% of the Caucasian population. Associations with alleles from the HLA class I region (now known as PSORS1), particularly HLA-Cw*0602, were described over 20 years ago. However, extensive linkage disequilibrium (LD) within this region has made it difficult to identify the true susceptibility allele from this region. A variety of genes and regions from a 238-kb interval extending from HLA-B to corneodesmosin (CDSN) have been proposed to harbor PSORS1. In order to identify the minimum block of LD in the MHC class I region associated with psoriasis we performed a comprehensive case/control and family-based association study on 242 Northern European psoriasis families and two separate European control populations. High resolution HLA typing of HLA-A, -B and -C alleles was performed, in addition to the genotyping of 18 polymorphic microsatellites and 36 SNPs from a 772-kb segment of the HLA class I region harboring the previously described interval. This corresponded on average to one SNP every 7 kb in the candidate 238 kb region. With all tests, the association was the strongest with single markers and haplotypes from a block of LD harboring HLA-C and SNP n.9. Logistic regression analyses indicated that association seen with candidate genes from the interval such as CDSN and HCR was entirely dependent on association with HLA-Cw*0602 and SNP n.9-G alleles. The previously reported association with CDSN and HCR was observed to be due to the existence of the associated alleles lying on the most commonly over-transmitted haplotype. Rare over-transmitted haplotypes also harbored HLA-Cw*12 alleles. HLA-Cw*12 family members are closely related to HLA Cw*0602, sharing identical sequences in their alpha-2 domains, peptide-binding pockets A, D and E and all 3′ introns. The introduction of a potential binding site for the RUNX/AML family of transcription factors in intron 7, is also specific to these HLA-C alleles. These variants need to be investigated further for their role as PSORS1.
Url:
DOI: 10.1007/s00439-005-0048-2
Affiliations:
- États-Unis
- District de Columbia, Missouri (État), Texas, État de New York
- Dallas, Saint-Louis (Missouri)
- École de médecine (Université Washington de Saint-Louis)
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Fernandez-Vina</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Oncology Department, Georgetown University School of Medicine, Washington, DC</wicri:regionArea><placeName><region type="state">District de Columbia</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Laboratory Medicine, The University of Texas M.D. Anderson, Cancer Center, Houston, TX</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Kwok, Pui Yan" sort="Kwok, Pui Yan" uniqKey="Kwok P" first="Pui-Yan" last="Kwok">Pui-Yan Kwok</name><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Dermatology, Department of Medicine, Washington University School of Medicine, St. Louis</wicri:regionArea><orgName type="university">École de médecine (Université Washington de Saint-Louis)</orgName><placeName><settlement type="city">Saint-Louis (Missouri)</settlement><region type="state">Missouri (État)</region></placeName></affiliation></author><author><name sortKey="Menter, Alan" sort="Menter, Alan" uniqKey="Menter A" first="Alan" last="Menter">Alan Menter</name><affiliation wicri:level="3"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Internal Medicine, Division of Dermatology, Baylor University Medical Center, Dallas</wicri:regionArea><placeName><settlement type="city">Dallas</settlement><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Bowcock, Anne M" sort="Bowcock, Anne M" uniqKey="Bowcock A" first="Anne M." last="Bowcock">Anne M. Bowcock</name><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Genetics, Washington University School of Medicine, 4566 Scott Avenue, Box 8232, 63110, St. Louis, Missouri</wicri:regionArea><placeName><region type="state">Missouri (État)</region><settlement type="city">Saint-Louis (Missouri)</settlement></placeName><orgName type="university">École de médecine (Université Washington de Saint-Louis)</orgName></affiliation><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Dermatology, Department of Medicine, Washington University School of Medicine, St. Louis</wicri:regionArea><orgName type="university">École de médecine (Université Washington de Saint-Louis)</orgName><placeName><settlement type="city">Saint-Louis (Missouri)</settlement><region type="state">Missouri (État)</region></placeName></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation></author></analytic><monogr></monogr><series><title level="j">Human Genetics</title><title level="j" type="abbrev">Hum Genet</title><idno type="ISSN">0340-6717</idno><idno type="eISSN">1432-1203</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="2005-12-01">2005-12-01</date><biblScope unit="volume">118</biblScope><biblScope unit="issue">3-4</biblScope><biblScope unit="page" from="466">466</biblScope><biblScope unit="page" to="476">476</biblScope></imprint><idno type="ISSN">0340-6717</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0340-6717</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Psoriasis is a complex inflammatory disease of the skin affecting 1–2% of the Caucasian population. Associations with alleles from the HLA class I region (now known as PSORS1), particularly HLA-Cw*0602, were described over 20 years ago. However, extensive linkage disequilibrium (LD) within this region has made it difficult to identify the true susceptibility allele from this region. A variety of genes and regions from a 238-kb interval extending from HLA-B to corneodesmosin (CDSN) have been proposed to harbor PSORS1. In order to identify the minimum block of LD in the MHC class I region associated with psoriasis we performed a comprehensive case/control and family-based association study on 242 Northern European psoriasis families and two separate European control populations. High resolution HLA typing of HLA-A, -B and -C alleles was performed, in addition to the genotyping of 18 polymorphic microsatellites and 36 SNPs from a 772-kb segment of the HLA class I region harboring the previously described interval. This corresponded on average to one SNP every 7 kb in the candidate 238 kb region. With all tests, the association was the strongest with single markers and haplotypes from a block of LD harboring HLA-C and SNP n.9. Logistic regression analyses indicated that association seen with candidate genes from the interval such as CDSN and HCR was entirely dependent on association with HLA-Cw*0602 and SNP n.9-G alleles. The previously reported association with CDSN and HCR was observed to be due to the existence of the associated alleles lying on the most commonly over-transmitted haplotype. Rare over-transmitted haplotypes also harbored HLA-Cw*12 alleles. HLA-Cw*12 family members are closely related to HLA Cw*0602, sharing identical sequences in their alpha-2 domains, peptide-binding pockets A, D and E and all 3′ introns. The introduction of a potential binding site for the RUNX/AML family of transcription factors in intron 7, is also specific to these HLA-C alleles. These variants need to be investigated further for their role as PSORS1.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>District de Columbia</li><li>Missouri (État)</li><li>Texas</li><li>État de New York</li></region><settlement><li>Dallas</li><li>Saint-Louis (Missouri)</li></settlement><orgName><li>École de médecine (Université Washington de Saint-Louis)</li></orgName></list><tree><country name="États-Unis"><region name="Missouri (État)"><name sortKey="Helms, Cynthia" sort="Helms, Cynthia" uniqKey="Helms C" first="Cynthia" last="Helms">Cynthia Helms</name></region><name sortKey="Bowcock, Anne M" sort="Bowcock, Anne M" uniqKey="Bowcock A" first="Anne M." last="Bowcock">Anne M. Bowcock</name><name sortKey="Bowcock, Anne M" sort="Bowcock, Anne M" uniqKey="Bowcock A" first="Anne M." last="Bowcock">Anne M. Bowcock</name><name sortKey="Bowcock, Anne M" sort="Bowcock, Anne M" uniqKey="Bowcock A" first="Anne M." last="Bowcock">Anne M. Bowcock</name><name sortKey="Cao, Kai" sort="Cao, Kai" uniqKey="Cao K" first="Kai" last="Cao">Kai Cao</name><name sortKey="Cao, Kai" sort="Cao, Kai" uniqKey="Cao K" first="Kai" last="Cao">Kai Cao</name><name sortKey="Cao, Li" sort="Cao, Li" uniqKey="Cao L" first="Li" last="Cao">Li Cao</name><name sortKey="Daw, Jil A Wright" sort="Daw, Jil A Wright" uniqKey="Daw J" first="Jil A. Wright." last="Daw">Jil A. Wright. Daw</name><name sortKey="Duan, Shenghui" sort="Duan, Shenghui" uniqKey="Duan S" first="Shenghui" last="Duan">Shenghui Duan</name><name sortKey="Fernandez Vina, Marcelo A" sort="Fernandez Vina, Marcelo A" uniqKey="Fernandez Vina M" first="Marcelo A." last="Fernandez-Vina">Marcelo A. Fernandez-Vina</name><name sortKey="Fernandez Vina, Marcelo A" sort="Fernandez Vina, Marcelo A" uniqKey="Fernandez Vina M" first="Marcelo A." last="Fernandez-Vina">Marcelo A. Fernandez-Vina</name><name sortKey="Gordon, Derek" sort="Gordon, Derek" uniqKey="Gordon D" first="Derek" last="Gordon">Derek Gordon</name><name sortKey="Hsu, Tony M" sort="Hsu, Tony M" uniqKey="Hsu T" first="Tony M." last="Hsu">Tony M. Hsu</name><name sortKey="Kwok, Pui Yan" sort="Kwok, Pui Yan" uniqKey="Kwok P" first="Pui-Yan" last="Kwok">Pui-Yan Kwok</name><name sortKey="Menter, Alan" sort="Menter, Alan" uniqKey="Menter A" first="Alan" last="Menter">Alan Menter</name><name sortKey="Ott, Jurg" sort="Ott, Jurg" uniqKey="Ott J" first="Jurg" last="Ott">Jurg Ott</name><name sortKey="Pierce, Brandon" sort="Pierce, Brandon" uniqKey="Pierce B" first="Brandon" last="Pierce">Brandon Pierce</name><name sortKey="Rice, John" sort="Rice, John" uniqKey="Rice J" first="John" last="Rice">John Rice</name><name sortKey="Saccone, Nancy L" sort="Saccone, Nancy L" uniqKey="Saccone N" first="Nancy L." last="Saccone">Nancy L. Saccone</name><name sortKey="Saccone, Nancy L" sort="Saccone, Nancy L" uniqKey="Saccone N" first="Nancy L." last="Saccone">Nancy L. Saccone</name><name sortKey="Taillon Miller, Patricia" sort="Taillon Miller, Patricia" uniqKey="Taillon Miller P" first="Patricia" last="Taillon-Miller">Patricia Taillon-Miller</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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