Publication:
Coexistence of HLA-B*08 and HLA-B*18 in Four Siblings with Lichen Sclerosus

dc.authorscopusid6603682965
dc.authorscopusid7004347982
dc.authorscopusid6701577980
dc.authorscopusid35579498900
dc.authorscopusid6601978714
dc.authorscopusid7003532093
dc.authorscopusid7003532093
dc.contributor.authorŞentürk, N.
dc.contributor.authorAydin, F.
dc.contributor.authorBirinci, A.
dc.contributor.authorYíldíz, L.
dc.contributor.authorCantürk, T.
dc.contributor.authorDurupínar, B.
dc.contributor.authorTuranli, A.Y.
dc.date.accessioned2020-06-21T15:43:29Z
dc.date.available2020-06-21T15:43:29Z
dc.date.issued2004
dc.departmentOndokuz Mayıs Üniversitesien_US
dc.department-temp[Şentürk] Nilgün, Department of Dermatology, Ondokuz Mayis Üniversitesi, Samsun, Turkey, Department of Dermatology, Ondokuz Mayis Üniversitesi, Samsun, Turkey; [Aydin] Fatma, Department of Dermatology, Ondokuz Mayis Üniversitesi, Samsun, Turkey; [Birinci] Asuman, Department of Microbiology, Ondokuz Mayis Üniversitesi, Samsun, Turkey; [Yíldíz] Levent, Department of Pathology, Ondokuz Mayis Üniversitesi, Samsun, Turkey; [Cantürk] Tayyar, Department of Dermatology, Ondokuz Mayis Üniversitesi, Samsun, Turkey; [Durupínar] Belma, Department of Microbiology, Ondokuz Mayis Üniversitesi, Samsun, Turkey; [Turanli] Ahmet Yaşar, Department of Dermatology, Ondokuz Mayis Üniversitesi, Samsun, Turkeyen_US
dc.description.abstractBackground: Lichen sclerosus (LS), is characterized by localized patches of atrophy and whitening of the skin. The cause of LS remains unknown, but genetic, hormonal, immunologic factors and autoimmune mechanisms have been incriminated. There are conflicting data regarding the association between LS and human leukocyte antigens (HLA). Methods: We have analyzed the HLA alleles of a family, in which 4 of 5 children have lichen sclerosus. Results: HLA-B*08 and HLA-B*18 alleles were detected in children with LS, but not in a healthy sister. None of the patients had autoimmune disease. Conclusion: In our opinion, coexistence of these two alleles may play a role in the development of LS. Copyright © 2004 S. Karger AG, Basel.en_US
dc.identifier.doi10.1159/000075049
dc.identifier.endpage66en_US
dc.identifier.issn1018-8665
dc.identifier.issn1421-9832
dc.identifier.issue1en_US
dc.identifier.pmid14730240
dc.identifier.scopus2-s2.0-0942300675
dc.identifier.scopusqualityQ1
dc.identifier.startpage64en_US
dc.identifier.urihttps://doi.org/10.1159/000075049
dc.identifier.urihttps://hdl.handle.net/20.500.12712/21635
dc.identifier.volume208en_US
dc.identifier.wosWOS:000188210300013
dc.identifier.wosqualityQ2
dc.language.isoenen_US
dc.publisherKargeren_US
dc.relation.ispartofDermatologyen_US
dc.relation.journalDermatologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAutoimmunityen_US
dc.subjectGeneticsen_US
dc.subjectHuman Leukocyte Antigensen_US
dc.subjectLichen Sclerosusen_US
dc.titleCoexistence of HLA-B*08 and HLA-B*18 in Four Siblings with Lichen Sclerosusen_US
dc.typeArticleen_US
dspace.entity.typePublication

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