Human leukocyte antigen system associations in Malassezia-related skin diseases

Background The human leukocyte antigen system (HLA) is divided into two classes involved in antigen presentation: class I presenting intracellular antigens and class II presenting extracellular antigens. While susceptibility to infections is correlated with the HLA system, data on associations betwe...

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Veröffentlicht in:Archives of dermatological research 2023-05, Vol.315 (4), p.895-902
Hauptverfasser: Lindsø Andersen, P., Jemec, G. B., Erikstrup, C., Didriksen, M., Dinh, K. M., Mikkelsen, S., Sørensen, E., Nielsen, K. R., Bruun, M. T., Hjalgrim, H., Hansen, T. F., Sækmose, S. G., Ostrowski, S. R., Saunte, D. M. L., Pedersen, O. B.
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container_end_page 902
container_issue 4
container_start_page 895
container_title Archives of dermatological research
container_volume 315
creator Lindsø Andersen, P.
Jemec, G. B.
Erikstrup, C.
Didriksen, M.
Dinh, K. M.
Mikkelsen, S.
Sørensen, E.
Nielsen, K. R.
Bruun, M. T.
Hjalgrim, H.
Hansen, T. F.
Sækmose, S. G.
Ostrowski, S. R.
Saunte, D. M. L.
Pedersen, O. B.
description Background The human leukocyte antigen system (HLA) is divided into two classes involved in antigen presentation: class I presenting intracellular antigens and class II presenting extracellular antigens. While susceptibility to infections is correlated with the HLA system, data on associations between HLA genotypes and Malassezia- related skin diseases (MRSD) are lacking. Thus, the objective of this study was to investigate associations between HLA alleles and MRSD. Materials and methods Participants in The Danish Blood Donor Study (2010–2018) provided questionnaire data on life style, anthropometric measures, and registry data on filled prescriptions. Genotyping was done using Illumina Infinium Global Screening Array, and HLA alleles were imputed using the HIBAG algorithm. Cases and controls were defined using filled prescriptions on topical ketoconazole 2% as a proxy of MRSD. Logistic regressions assessed associations between HLA alleles and MRSD adjusted for confounders and Bonferroni corrected for multiple tests. Results A total of 9455 participants were considered MRSD cases and 24,144 participants as controls. We identified four risk alleles B*57:01, OR 1.19 (95% CI: 1.09–1.31), C*01:02, OR 1.19 (95% CI: 1.08–1.32), C*06:02, OR 1.14 (95% CI: 1.08–1.22), and DRB1*01:01, OR 1.10 (95% CI: 1.04–1.17), and two protective alleles, DQB1*02:01, OR 0.89 (95% CI: 0.85–0.94), and DRB1*03:01, OR 0.89 (95% CI: 0.85–0.94). Conclusion Five novel associations between HLA alleles and MRSD were identified in our cohort, and one previous association was confirmed. Future studies should assess the correlation between Malassezia antigens and antigen-binding properties of the associated HLA alleles.
doi_str_mv 10.1007/s00403-022-02454-9
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B. ; Erikstrup, C. ; Didriksen, M. ; Dinh, K. M. ; Mikkelsen, S. ; Sørensen, E. ; Nielsen, K. R. ; Bruun, M. T. ; Hjalgrim, H. ; Hansen, T. F. ; Sækmose, S. G. ; Ostrowski, S. R. ; Saunte, D. M. L. ; Pedersen, O. B.</creator><creatorcontrib>Lindsø Andersen, P. ; Jemec, G. B. ; Erikstrup, C. ; Didriksen, M. ; Dinh, K. M. ; Mikkelsen, S. ; Sørensen, E. ; Nielsen, K. R. ; Bruun, M. T. ; Hjalgrim, H. ; Hansen, T. F. ; Sækmose, S. G. ; Ostrowski, S. R. ; Saunte, D. M. L. ; Pedersen, O. B. ; DBDS Genetic Consortium</creatorcontrib><description>Background The human leukocyte antigen system (HLA) is divided into two classes involved in antigen presentation: class I presenting intracellular antigens and class II presenting extracellular antigens. While susceptibility to infections is correlated with the HLA system, data on associations between HLA genotypes and Malassezia- related skin diseases (MRSD) are lacking. Thus, the objective of this study was to investigate associations between HLA alleles and MRSD. Materials and methods Participants in The Danish Blood Donor Study (2010–2018) provided questionnaire data on life style, anthropometric measures, and registry data on filled prescriptions. Genotyping was done using Illumina Infinium Global Screening Array, and HLA alleles were imputed using the HIBAG algorithm. Cases and controls were defined using filled prescriptions on topical ketoconazole 2% as a proxy of MRSD. Logistic regressions assessed associations between HLA alleles and MRSD adjusted for confounders and Bonferroni corrected for multiple tests. Results A total of 9455 participants were considered MRSD cases and 24,144 participants as controls. We identified four risk alleles B*57:01, OR 1.19 (95% CI: 1.09–1.31), C*01:02, OR 1.19 (95% CI: 1.08–1.32), C*06:02, OR 1.14 (95% CI: 1.08–1.22), and DRB1*01:01, OR 1.10 (95% CI: 1.04–1.17), and two protective alleles, DQB1*02:01, OR 0.89 (95% CI: 0.85–0.94), and DRB1*03:01, OR 0.89 (95% CI: 0.85–0.94). Conclusion Five novel associations between HLA alleles and MRSD were identified in our cohort, and one previous association was confirmed. Future studies should assess the correlation between Malassezia antigens and antigen-binding properties of the associated HLA alleles.</description><identifier>ISSN: 1432-069X</identifier><identifier>ISSN: 0340-3696</identifier><identifier>EISSN: 1432-069X</identifier><identifier>DOI: 10.1007/s00403-022-02454-9</identifier><identifier>PMID: 36394635</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adult ; Alleles ; Antifungal agents ; Antigen presentation ; Antigens ; Blood Donors ; Case-Control Studies ; Cohort Studies ; Denmark ; Dermatology ; Dermatomycoses - blood ; Dermatomycoses - genetics ; Drb1 protein ; Female ; Genotype ; Genotypes ; Genotyping ; Histocompatibility antigen HLA ; HLA Antigens - genetics ; Humans ; Ketoconazole ; Leukocytes ; Malassezia ; Malassezia - genetics ; Male ; Medicine ; Medicine &amp; Public Health ; Middle Aged ; Original Paper ; Skin diseases ; Skin Diseases, Genetic</subject><ispartof>Archives of dermatological research, 2023-05, Vol.315 (4), p.895-902</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022. 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The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-5e5f39f36bebaab033de90e1f256267d018e49921ae3293c2583c934cbe969563</citedby><cites>FETCH-LOGICAL-c375t-5e5f39f36bebaab033de90e1f256267d018e49921ae3293c2583c934cbe969563</cites><orcidid>0000-0003-1881-5673 ; 0000-0002-4856-496X ; 0000-0001-7806-1143 ; 0000-0002-8819-5388 ; 0000-0002-4436-6798 ; 0000-0002-0132-4715 ; 0000-0002-0712-2540 ; 0000-0001-6703-7762 ; 0000-0001-7953-1047 ; 0000-0001-6551-6647 ; 0000-0003-2312-5976 ; 0000-0002-1346-0052 ; 0000-0001-5288-3851</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00403-022-02454-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00403-022-02454-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36394635$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lindsø Andersen, P.</creatorcontrib><creatorcontrib>Jemec, G. B.</creatorcontrib><creatorcontrib>Erikstrup, C.</creatorcontrib><creatorcontrib>Didriksen, M.</creatorcontrib><creatorcontrib>Dinh, K. M.</creatorcontrib><creatorcontrib>Mikkelsen, S.</creatorcontrib><creatorcontrib>Sørensen, E.</creatorcontrib><creatorcontrib>Nielsen, K. R.</creatorcontrib><creatorcontrib>Bruun, M. T.</creatorcontrib><creatorcontrib>Hjalgrim, H.</creatorcontrib><creatorcontrib>Hansen, T. F.</creatorcontrib><creatorcontrib>Sækmose, S. G.</creatorcontrib><creatorcontrib>Ostrowski, S. R.</creatorcontrib><creatorcontrib>Saunte, D. M. L.</creatorcontrib><creatorcontrib>Pedersen, O. B.</creatorcontrib><creatorcontrib>DBDS Genetic Consortium</creatorcontrib><title>Human leukocyte antigen system associations in Malassezia-related skin diseases</title><title>Archives of dermatological research</title><addtitle>Arch Dermatol Res</addtitle><addtitle>Arch Dermatol Res</addtitle><description>Background The human leukocyte antigen system (HLA) is divided into two classes involved in antigen presentation: class I presenting intracellular antigens and class II presenting extracellular antigens. While susceptibility to infections is correlated with the HLA system, data on associations between HLA genotypes and Malassezia- related skin diseases (MRSD) are lacking. Thus, the objective of this study was to investigate associations between HLA alleles and MRSD. Materials and methods Participants in The Danish Blood Donor Study (2010–2018) provided questionnaire data on life style, anthropometric measures, and registry data on filled prescriptions. Genotyping was done using Illumina Infinium Global Screening Array, and HLA alleles were imputed using the HIBAG algorithm. Cases and controls were defined using filled prescriptions on topical ketoconazole 2% as a proxy of MRSD. Logistic regressions assessed associations between HLA alleles and MRSD adjusted for confounders and Bonferroni corrected for multiple tests. Results A total of 9455 participants were considered MRSD cases and 24,144 participants as controls. We identified four risk alleles B*57:01, OR 1.19 (95% CI: 1.09–1.31), C*01:02, OR 1.19 (95% CI: 1.08–1.32), C*06:02, OR 1.14 (95% CI: 1.08–1.22), and DRB1*01:01, OR 1.10 (95% CI: 1.04–1.17), and two protective alleles, DQB1*02:01, OR 0.89 (95% CI: 0.85–0.94), and DRB1*03:01, OR 0.89 (95% CI: 0.85–0.94). Conclusion Five novel associations between HLA alleles and MRSD were identified in our cohort, and one previous association was confirmed. Future studies should assess the correlation between Malassezia antigens and antigen-binding properties of the associated HLA alleles.</description><subject>Adult</subject><subject>Alleles</subject><subject>Antifungal agents</subject><subject>Antigen presentation</subject><subject>Antigens</subject><subject>Blood Donors</subject><subject>Case-Control Studies</subject><subject>Cohort Studies</subject><subject>Denmark</subject><subject>Dermatology</subject><subject>Dermatomycoses - blood</subject><subject>Dermatomycoses - genetics</subject><subject>Drb1 protein</subject><subject>Female</subject><subject>Genotype</subject><subject>Genotypes</subject><subject>Genotyping</subject><subject>Histocompatibility antigen HLA</subject><subject>HLA Antigens - genetics</subject><subject>Humans</subject><subject>Ketoconazole</subject><subject>Leukocytes</subject><subject>Malassezia</subject><subject>Malassezia - genetics</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine &amp; Public Health</subject><subject>Middle Aged</subject><subject>Original Paper</subject><subject>Skin diseases</subject><subject>Skin Diseases, Genetic</subject><issn>1432-069X</issn><issn>0340-3696</issn><issn>1432-069X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kD1PwzAQhi0EoqXwBxhQJBaWgO1znHpECChSUReQ2CwnuVRp81FyyVB-PYaUDzEwWOe7e97X1svYqeCXgvP4ijhXHEIupT8qUqHZY2OhwLfavOz_uo_YEdGKe1E8FYdsBBqM0hCN2WLWV64OSuzXTbrtMHB1VyyxDmhLHVaBI2rSwnVFU1NQ1MGjK_0I3woXtli6DrOA1n6eFYSOkI7ZQe5KwpNdnbDnu9unm1k4X9w_3FzPwxTiqAsjjHIwOegEE-cSDpCh4ShyGWmp44yLKSpjpHAI0kAqoymkBlSaoNEm0jBhF4Pvpm1ee6TOVgWlWJauxqYnK2OIVSyklh49_4Oumr6t_e88ZYzgsVHCU3Kg0rYhajG3m7aoXLu1gtuPuO0Qt_Vx28-4rfGis511n1SYfUu-8vUADAD5Vb3E9uftf2zfAaZVinc</recordid><startdate>20230501</startdate><enddate>20230501</enddate><creator>Lindsø Andersen, P.</creator><creator>Jemec, G. 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M. L.</au><au>Pedersen, O. B.</au><aucorp>DBDS Genetic Consortium</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human leukocyte antigen system associations in Malassezia-related skin diseases</atitle><jtitle>Archives of dermatological research</jtitle><stitle>Arch Dermatol Res</stitle><addtitle>Arch Dermatol Res</addtitle><date>2023-05-01</date><risdate>2023</risdate><volume>315</volume><issue>4</issue><spage>895</spage><epage>902</epage><pages>895-902</pages><issn>1432-069X</issn><issn>0340-3696</issn><eissn>1432-069X</eissn><abstract>Background The human leukocyte antigen system (HLA) is divided into two classes involved in antigen presentation: class I presenting intracellular antigens and class II presenting extracellular antigens. While susceptibility to infections is correlated with the HLA system, data on associations between HLA genotypes and Malassezia- related skin diseases (MRSD) are lacking. Thus, the objective of this study was to investigate associations between HLA alleles and MRSD. Materials and methods Participants in The Danish Blood Donor Study (2010–2018) provided questionnaire data on life style, anthropometric measures, and registry data on filled prescriptions. Genotyping was done using Illumina Infinium Global Screening Array, and HLA alleles were imputed using the HIBAG algorithm. Cases and controls were defined using filled prescriptions on topical ketoconazole 2% as a proxy of MRSD. Logistic regressions assessed associations between HLA alleles and MRSD adjusted for confounders and Bonferroni corrected for multiple tests. Results A total of 9455 participants were considered MRSD cases and 24,144 participants as controls. We identified four risk alleles B*57:01, OR 1.19 (95% CI: 1.09–1.31), C*01:02, OR 1.19 (95% CI: 1.08–1.32), C*06:02, OR 1.14 (95% CI: 1.08–1.22), and DRB1*01:01, OR 1.10 (95% CI: 1.04–1.17), and two protective alleles, DQB1*02:01, OR 0.89 (95% CI: 0.85–0.94), and DRB1*03:01, OR 0.89 (95% CI: 0.85–0.94). Conclusion Five novel associations between HLA alleles and MRSD were identified in our cohort, and one previous association was confirmed. Future studies should assess the correlation between Malassezia antigens and antigen-binding properties of the associated HLA alleles.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>36394635</pmid><doi>10.1007/s00403-022-02454-9</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-1881-5673</orcidid><orcidid>https://orcid.org/0000-0002-4856-496X</orcidid><orcidid>https://orcid.org/0000-0001-7806-1143</orcidid><orcidid>https://orcid.org/0000-0002-8819-5388</orcidid><orcidid>https://orcid.org/0000-0002-4436-6798</orcidid><orcidid>https://orcid.org/0000-0002-0132-4715</orcidid><orcidid>https://orcid.org/0000-0002-0712-2540</orcidid><orcidid>https://orcid.org/0000-0001-6703-7762</orcidid><orcidid>https://orcid.org/0000-0001-7953-1047</orcidid><orcidid>https://orcid.org/0000-0001-6551-6647</orcidid><orcidid>https://orcid.org/0000-0003-2312-5976</orcidid><orcidid>https://orcid.org/0000-0002-1346-0052</orcidid><orcidid>https://orcid.org/0000-0001-5288-3851</orcidid></addata></record>
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source MEDLINE; Springer Nature - Complete Springer Journals
subjects Adult
Alleles
Antifungal agents
Antigen presentation
Antigens
Blood Donors
Case-Control Studies
Cohort Studies
Denmark
Dermatology
Dermatomycoses - blood
Dermatomycoses - genetics
Drb1 protein
Female
Genotype
Genotypes
Genotyping
Histocompatibility antigen HLA
HLA Antigens - genetics
Humans
Ketoconazole
Leukocytes
Malassezia
Malassezia - genetics
Male
Medicine
Medicine & Public Health
Middle Aged
Original Paper
Skin diseases
Skin Diseases, Genetic
title Human leukocyte antigen system associations in Malassezia-related skin diseases
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