Specific HLA genotypes confer susceptibility to acute necrotizing encephalopathy
Acute necrotizing encephalopathy (ANE) is a rare and severe syndrome of acute encephalopathy triggered by viral infections. Cytokine storm is considered as the main pathogenetic mechanism of ANE. ANE is prevalent in East Asia, suggesting the association of host genetic factors. To elucidate the gene...
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| Veröffentlicht in: | Genes and immunity 2016-09, Vol.17 (6), p.367-369 |
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| creator | Hoshino, A Saitoh, M Miyagawa, T Kubota, M Takanashi, J-i Miyamoto, A Tokunaga, K Oka, A Mizuguchi, M |
| description | Acute necrotizing encephalopathy (ANE) is a rare and severe syndrome of acute encephalopathy triggered by viral infections. Cytokine storm is considered as the main pathogenetic mechanism of ANE. ANE is prevalent in East Asia, suggesting the association of host genetic factors. To elucidate the genetic background of Japanese ANE, we examined genotypes of
human leukocyte antigen
(
HLA
)
-A, C, B, DRB1, DQB1 and DPB1
in 31 patients. Significant positive association was observed in both the allele frequency and positivity of
DRB1*09:01
(
P
=0.043 and 0.025, respectively), as well as those of
DQB1*03:03
(
P
=0.034 and 0.026, respectively). The carrier frequency of
DRB1*09:01
and
DQB1*03:03
alleles was higher in the patients (45.16%) than in controls (28.57%). These alleles are more common in East Asian than in European populations, and are reportedly associated with various autoimmune diseases in Japanese patients. Our data provide further evidence that altered immune response based on individual
HLA
genotypes may contribute to ANE pathogenesis. |
| doi_str_mv | 10.1038/gene.2016.32 |
| format | Article |
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human leukocyte antigen
(
HLA
)
-A, C, B, DRB1, DQB1 and DPB1
in 31 patients. Significant positive association was observed in both the allele frequency and positivity of
DRB1*09:01
(
P
=0.043 and 0.025, respectively), as well as those of
DQB1*03:03
(
P
=0.034 and 0.026, respectively). The carrier frequency of
DRB1*09:01
and
DQB1*03:03
alleles was higher in the patients (45.16%) than in controls (28.57%). These alleles are more common in East Asian than in European populations, and are reportedly associated with various autoimmune diseases in Japanese patients. Our data provide further evidence that altered immune response based on individual
HLA
genotypes may contribute to ANE pathogenesis.</description><identifier>ISSN: 1466-4879</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/gene.2016.32</identifier><identifier>PMID: 27467284</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>45/77 ; 631/208/205 ; 631/250/21/324 ; Alleles ; Autoimmune diseases ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Care and treatment ; Cytokine storm ; Cytokines ; Development and progression ; Disease Susceptibility ; Drb1 protein ; Encephalitis, Viral - genetics ; Encephalitis, Viral - pathology ; Encephalopathy ; Gene Expression ; Gene frequency ; Genetic aspects ; Genetic factors ; Genetic Predisposition to Disease ; Genotype ; Genotypes ; Health aspects ; Histocompatibility antigen HLA ; Histocompatibility antigens ; HLA Antigens - genetics ; HLA histocompatibility antigens ; Human Genetics ; Humans ; Immune response ; Immunology ; Leigh disease ; Leukoencephalitis, Acute Hemorrhagic - genetics ; Population genetics ; short-communication</subject><ispartof>Genes and immunity, 2016-09, Vol.17 (6), p.367-369</ispartof><rights>Macmillan Publishers Limited, part of Springer Nature. 2016</rights><rights>COPYRIGHT 2016 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Sep 2016</rights><rights>Macmillan Publishers Limited, part of Springer Nature. 2016.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-a9369ccacbf1282d5c29c869ad8694d7a3c39505262fcc94d0003b38efe25d283</citedby><cites>FETCH-LOGICAL-c490t-a9369ccacbf1282d5c29c869ad8694d7a3c39505262fcc94d0003b38efe25d283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/gene.2016.32$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/gene.2016.32$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27467284$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hoshino, A</creatorcontrib><creatorcontrib>Saitoh, M</creatorcontrib><creatorcontrib>Miyagawa, T</creatorcontrib><creatorcontrib>Kubota, M</creatorcontrib><creatorcontrib>Takanashi, J-i</creatorcontrib><creatorcontrib>Miyamoto, A</creatorcontrib><creatorcontrib>Tokunaga, K</creatorcontrib><creatorcontrib>Oka, A</creatorcontrib><creatorcontrib>Mizuguchi, M</creatorcontrib><title>Specific HLA genotypes confer susceptibility to acute necrotizing encephalopathy</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><addtitle>Genes Immun</addtitle><description>Acute necrotizing encephalopathy (ANE) is a rare and severe syndrome of acute encephalopathy triggered by viral infections. Cytokine storm is considered as the main pathogenetic mechanism of ANE. ANE is prevalent in East Asia, suggesting the association of host genetic factors. To elucidate the genetic background of Japanese ANE, we examined genotypes of
human leukocyte antigen
(
HLA
)
-A, C, B, DRB1, DQB1 and DPB1
in 31 patients. Significant positive association was observed in both the allele frequency and positivity of
DRB1*09:01
(
P
=0.043 and 0.025, respectively), as well as those of
DQB1*03:03
(
P
=0.034 and 0.026, respectively). The carrier frequency of
DRB1*09:01
and
DQB1*03:03
alleles was higher in the patients (45.16%) than in controls (28.57%). These alleles are more common in East Asian than in European populations, and are reportedly associated with various autoimmune diseases in Japanese patients. Our data provide further evidence that altered immune response based on individual
HLA
genotypes may contribute to ANE pathogenesis.</description><subject>45/77</subject><subject>631/208/205</subject><subject>631/250/21/324</subject><subject>Alleles</subject><subject>Autoimmune diseases</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Care and treatment</subject><subject>Cytokine storm</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Disease Susceptibility</subject><subject>Drb1 protein</subject><subject>Encephalitis, Viral - genetics</subject><subject>Encephalitis, Viral - pathology</subject><subject>Encephalopathy</subject><subject>Gene Expression</subject><subject>Gene frequency</subject><subject>Genetic aspects</subject><subject>Genetic factors</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Genotypes</subject><subject>Health aspects</subject><subject>Histocompatibility antigen HLA</subject><subject>Histocompatibility antigens</subject><subject>HLA Antigens - genetics</subject><subject>HLA histocompatibility antigens</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunology</subject><subject>Leigh disease</subject><subject>Leukoencephalitis, Acute Hemorrhagic - genetics</subject><subject>Population genetics</subject><subject>short-communication</subject><issn>1466-4879</issn><issn>1476-5470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqN0dtrFDEUB-Agir3om88y4IuCs-Z-eVyKtoWFFqvPIZs5M02ZzYyTDHT9682wVUoR8SUJycfhl3MQekPwimCmP3UQYUUxkStGn6FjwpWsBVf4-XKWsuZamSN0ktIdLohI8xIdUcWlopofo-ubEXxog68uNuuq1BryfoRU-SG2MFVpTh7GHLahD3lf5aFyfs5QRfDTkMPPELsKYiG3rh9Gl2_3r9CL1vUJXj_sp-j7l8_fzi7qzdX55dl6U3tucK6dYdJ47_y2JVTTRnhqvJbGNWXhjXLMMyOwoJK23pcbjDHbMg0tUNFQzU7R-0PdcRp-zJCy3YWSte9dhGFOlmhiCBdckP-hUjJuFC703RN6N8xTLB-xVHKimFSF_kOVWkJqQdmS8MNBda4HG2JpaYb73Lk5JXt589WupcBYCo1VsR8PtrQ1pQlaO05h56a9JdguY7bLmO0yZsto4W8fAszbHTR_8O-5FlAfQCpPsYPpUcK_FfwF9bOwCw</recordid><startdate>20160901</startdate><enddate>20160901</enddate><creator>Hoshino, A</creator><creator>Saitoh, M</creator><creator>Miyagawa, T</creator><creator>Kubota, M</creator><creator>Takanashi, J-i</creator><creator>Miyamoto, A</creator><creator>Tokunaga, K</creator><creator>Oka, A</creator><creator>Mizuguchi, M</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISR</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20160901</creationdate><title>Specific HLA genotypes confer susceptibility to acute necrotizing encephalopathy</title><author>Hoshino, A ; Saitoh, M ; Miyagawa, T ; Kubota, M ; Takanashi, J-i ; Miyamoto, A ; Tokunaga, K ; Oka, A ; Mizuguchi, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-a9369ccacbf1282d5c29c869ad8694d7a3c39505262fcc94d0003b38efe25d283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>45/77</topic><topic>631/208/205</topic><topic>631/250/21/324</topic><topic>Alleles</topic><topic>Autoimmune diseases</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Care and treatment</topic><topic>Cytokine storm</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Disease Susceptibility</topic><topic>Drb1 protein</topic><topic>Encephalitis, Viral - genetics</topic><topic>Encephalitis, Viral - pathology</topic><topic>Encephalopathy</topic><topic>Gene Expression</topic><topic>Gene frequency</topic><topic>Genetic aspects</topic><topic>Genetic factors</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Genotypes</topic><topic>Health aspects</topic><topic>Histocompatibility antigen HLA</topic><topic>Histocompatibility antigens</topic><topic>HLA Antigens - genetics</topic><topic>HLA histocompatibility antigens</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immunology</topic><topic>Leigh disease</topic><topic>Leukoencephalitis, Acute Hemorrhagic - genetics</topic><topic>Population genetics</topic><topic>short-communication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hoshino, A</creatorcontrib><creatorcontrib>Saitoh, M</creatorcontrib><creatorcontrib>Miyagawa, T</creatorcontrib><creatorcontrib>Kubota, M</creatorcontrib><creatorcontrib>Takanashi, J-i</creatorcontrib><creatorcontrib>Miyamoto, A</creatorcontrib><creatorcontrib>Tokunaga, K</creatorcontrib><creatorcontrib>Oka, A</creatorcontrib><creatorcontrib>Mizuguchi, M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genes and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hoshino, A</au><au>Saitoh, M</au><au>Miyagawa, T</au><au>Kubota, M</au><au>Takanashi, J-i</au><au>Miyamoto, A</au><au>Tokunaga, K</au><au>Oka, A</au><au>Mizuguchi, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Specific HLA genotypes confer susceptibility to acute necrotizing encephalopathy</atitle><jtitle>Genes and immunity</jtitle><stitle>Genes Immun</stitle><addtitle>Genes Immun</addtitle><date>2016-09-01</date><risdate>2016</risdate><volume>17</volume><issue>6</issue><spage>367</spage><epage>369</epage><pages>367-369</pages><issn>1466-4879</issn><eissn>1476-5470</eissn><abstract>Acute necrotizing encephalopathy (ANE) is a rare and severe syndrome of acute encephalopathy triggered by viral infections. Cytokine storm is considered as the main pathogenetic mechanism of ANE. ANE is prevalent in East Asia, suggesting the association of host genetic factors. To elucidate the genetic background of Japanese ANE, we examined genotypes of
human leukocyte antigen
(
HLA
)
-A, C, B, DRB1, DQB1 and DPB1
in 31 patients. Significant positive association was observed in both the allele frequency and positivity of
DRB1*09:01
(
P
=0.043 and 0.025, respectively), as well as those of
DQB1*03:03
(
P
=0.034 and 0.026, respectively). The carrier frequency of
DRB1*09:01
and
DQB1*03:03
alleles was higher in the patients (45.16%) than in controls (28.57%). These alleles are more common in East Asian than in European populations, and are reportedly associated with various autoimmune diseases in Japanese patients. Our data provide further evidence that altered immune response based on individual
HLA
genotypes may contribute to ANE pathogenesis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27467284</pmid><doi>10.1038/gene.2016.32</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 45/77 631/208/205 631/250/21/324 Alleles Autoimmune diseases Biomedical and Life Sciences Biomedicine Cancer Research Care and treatment Cytokine storm Cytokines Development and progression Disease Susceptibility Drb1 protein Encephalitis, Viral - genetics Encephalitis, Viral - pathology Encephalopathy Gene Expression Gene frequency Genetic aspects Genetic factors Genetic Predisposition to Disease Genotype Genotypes Health aspects Histocompatibility antigen HLA Histocompatibility antigens HLA Antigens - genetics HLA histocompatibility antigens Human Genetics Humans Immune response Immunology Leigh disease Leukoencephalitis, Acute Hemorrhagic - genetics Population genetics short-communication |
| title | Specific HLA genotypes confer susceptibility to acute necrotizing encephalopathy |
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