Genetic involvement of bacterial sensor molecules in Japanese leprosy
Occurrence of new patients of leprosy, caused by Mycobacterium leprae infection, is now almost absent in Japan but is still uncontrolled in developing countries. As one factor affecting the disease development, genetic predisposition of a host has been considered to be associated. Actually, various...
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Veröffentlicht in: | JAPANESE JOURNAL OF LEPROSY 2009, Vol.78(3), pp.255-261 |
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creator | KANAZAWA, Nobuo MIKITA, Naoya LI, Hong-jin NAKATANI, Yumi OZAKI, Motoaki KOSAKA, Maki ISHII, Norihisa NISHIMURA, Hiroyuki FURUKAWA, Fukumi |
description | Occurrence of new patients of leprosy, caused by Mycobacterium leprae infection, is now almost absent in Japan but is still uncontrolled in developing countries. As one factor affecting the disease development, genetic predisposition of a host has been considered to be associated. Actually, various gene mutations have been reported to be associated at two stages of the disease progression, not only establishment of the disease but also determination of the phenotype, such as lepromatous (L)-type, tuberculoid (T)-type and reversal reaction. On the basis of recent progress of the research on innate immunity, here we analyzed single nucleotide polymorphisms (SNPs) of the genes of major bacterial sensor molecules expressed in antigen-presenting cells, TLR2 , DC-SIGN , NOD1 and NOD2 , in Japanese leprosy patients. As a result, frequency of polymorphisms in DC-SIGN -336 showed significant difference between the leprosy patients and the healthy controls, reflecting its role in establishment of the disease. Especially, among those with a particular TLR2 -16934 genotype, frequency of the polymorphisms in DC-SIGN -336 showed significant difference between the patients and the controls, suggesting any cooperation of these SNPs. |
doi_str_mv | 10.5025/hansen.78.255 |
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As one factor affecting the disease development, genetic predisposition of a host has been considered to be associated. Actually, various gene mutations have been reported to be associated at two stages of the disease progression, not only establishment of the disease but also determination of the phenotype, such as lepromatous (L)-type, tuberculoid (T)-type and reversal reaction. On the basis of recent progress of the research on innate immunity, here we analyzed single nucleotide polymorphisms (SNPs) of the genes of major bacterial sensor molecules expressed in antigen-presenting cells, TLR2 , DC-SIGN , NOD1 and NOD2 , in Japanese leprosy patients. As a result, frequency of polymorphisms in DC-SIGN -336 showed significant difference between the leprosy patients and the healthy controls, reflecting its role in establishment of the disease. Especially, among those with a particular TLR2 -16934 genotype, frequency of the polymorphisms in DC-SIGN -336 showed significant difference between the patients and the controls, suggesting any cooperation of these SNPs.</description><identifier>ISSN: 1342-3681</identifier><identifier>EISSN: 1884-314X</identifier><identifier>DOI: 10.5025/hansen.78.255</identifier><identifier>PMID: 19803376</identifier><language>eng ; jpn</language><publisher>Japan: Japanese Leprosy Association</publisher><subject>Antigen-Presenting Cells - immunology ; Asian Continental Ancestry Group ; bacterial sensor molecule ; Cell Adhesion Molecules - genetics ; gene polymorphism ; Genetic Predisposition to Disease - genetics ; Genotype ; Humans ; Immunity, Innate - genetics ; Japanese ; Lectins, C-Type - genetics ; leprosy ; Nod1 Signaling Adaptor Protein - genetics ; Nod2 Signaling Adaptor Protein - genetics ; Polymorphism, Single Nucleotide - genetics ; Receptors, Cell Surface - genetics ; Toll-Like Receptor 2 - genetics</subject><ispartof>JAPANESE JOURNAL OF LEPROSY, 2009, Vol.78(3), pp.255-261</ispartof><rights>2009 Japanese Leprosy Association</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3055-f32382ebe6266cba5e8d74bee84cfd74cc1be28a5d40cbc45b7ba1368a8d3c433</citedby><cites>FETCH-LOGICAL-c3055-f32382ebe6266cba5e8d74bee84cfd74cc1be28a5d40cbc45b7ba1368a8d3c433</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19803376$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KANAZAWA, Nobuo</creatorcontrib><creatorcontrib>MIKITA, Naoya</creatorcontrib><creatorcontrib>LI, Hong-jin</creatorcontrib><creatorcontrib>NAKATANI, Yumi</creatorcontrib><creatorcontrib>OZAKI, Motoaki</creatorcontrib><creatorcontrib>KOSAKA, Maki</creatorcontrib><creatorcontrib>ISHII, Norihisa</creatorcontrib><creatorcontrib>NISHIMURA, Hiroyuki</creatorcontrib><creatorcontrib>FURUKAWA, Fukumi</creatorcontrib><title>Genetic involvement of bacterial sensor molecules in Japanese leprosy</title><title>JAPANESE JOURNAL OF LEPROSY</title><addtitle>Jpn J Lepr</addtitle><description>Occurrence of new patients of leprosy, caused by Mycobacterium leprae infection, is now almost absent in Japan but is still uncontrolled in developing countries. As one factor affecting the disease development, genetic predisposition of a host has been considered to be associated. Actually, various gene mutations have been reported to be associated at two stages of the disease progression, not only establishment of the disease but also determination of the phenotype, such as lepromatous (L)-type, tuberculoid (T)-type and reversal reaction. On the basis of recent progress of the research on innate immunity, here we analyzed single nucleotide polymorphisms (SNPs) of the genes of major bacterial sensor molecules expressed in antigen-presenting cells, TLR2 , DC-SIGN , NOD1 and NOD2 , in Japanese leprosy patients. As a result, frequency of polymorphisms in DC-SIGN -336 showed significant difference between the leprosy patients and the healthy controls, reflecting its role in establishment of the disease. Especially, among those with a particular TLR2 -16934 genotype, frequency of the polymorphisms in DC-SIGN -336 showed significant difference between the patients and the controls, suggesting any cooperation of these SNPs.</description><subject>Antigen-Presenting Cells - immunology</subject><subject>Asian Continental Ancestry Group</subject><subject>bacterial sensor molecule</subject><subject>Cell Adhesion Molecules - genetics</subject><subject>gene polymorphism</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genotype</subject><subject>Humans</subject><subject>Immunity, Innate - genetics</subject><subject>Japanese</subject><subject>Lectins, C-Type - genetics</subject><subject>leprosy</subject><subject>Nod1 Signaling Adaptor Protein - genetics</subject><subject>Nod2 Signaling Adaptor Protein - genetics</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Toll-Like Receptor 2 - genetics</subject><issn>1342-3681</issn><issn>1884-314X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkM9LwzAYhoMobuiOXqU3T5352cSjjjmVgRcFbyFJv7pK2s6kHey_N9IxvSQf5OH93jwIXRE8F5iK241pI7RzqeZUiBM0JUrxnBH-cZpmxmnOCkUmaBZjbTGWsqAF4-doQu4UZkwWU7RcQQt97bK63XV-Bw20fdZVmTWuh1Abn6UFsQtZ03lwg4eYyOzFbE0LETIP29DF_SU6q4yPMDvcF-j9cfm2eMrXr6vnxf06dwwLkVeMMkXBQupROGsEqFJyC6C4q9LkHLFAlRElx846Lqy0hqQ_GFUyxxm7QDdjbtr6PUDsdVNHB96nNt0QtWQcSyo5TmQ-ki71iwEqvQ11Y8JeE6x_3enRnZZKJ3eJvz4kD7aB8o8-mErAwwh8xd58whEwIdnz8C-OjUdKPT66jQkaWvYDCJiE0w</recordid><startdate>200909</startdate><enddate>200909</enddate><creator>KANAZAWA, Nobuo</creator><creator>MIKITA, Naoya</creator><creator>LI, Hong-jin</creator><creator>NAKATANI, Yumi</creator><creator>OZAKI, Motoaki</creator><creator>KOSAKA, Maki</creator><creator>ISHII, Norihisa</creator><creator>NISHIMURA, Hiroyuki</creator><creator>FURUKAWA, Fukumi</creator><general>Japanese Leprosy Association</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>7X8</scope></search><sort><creationdate>200909</creationdate><title>Genetic involvement of bacterial sensor molecules in Japanese leprosy</title><author>KANAZAWA, Nobuo ; MIKITA, Naoya ; LI, Hong-jin ; NAKATANI, Yumi ; OZAKI, Motoaki ; KOSAKA, Maki ; ISHII, Norihisa ; NISHIMURA, Hiroyuki ; FURUKAWA, Fukumi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3055-f32382ebe6266cba5e8d74bee84cfd74cc1be28a5d40cbc45b7ba1368a8d3c433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng ; jpn</language><creationdate>2009</creationdate><topic>Antigen-Presenting Cells - immunology</topic><topic>Asian Continental Ancestry Group</topic><topic>bacterial sensor molecule</topic><topic>Cell Adhesion Molecules - genetics</topic><topic>gene polymorphism</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genotype</topic><topic>Humans</topic><topic>Immunity, Innate - genetics</topic><topic>Japanese</topic><topic>Lectins, C-Type - genetics</topic><topic>leprosy</topic><topic>Nod1 Signaling Adaptor Protein - genetics</topic><topic>Nod2 Signaling Adaptor Protein - genetics</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Toll-Like Receptor 2 - genetics</topic><toplevel>online_resources</toplevel><creatorcontrib>KANAZAWA, Nobuo</creatorcontrib><creatorcontrib>MIKITA, Naoya</creatorcontrib><creatorcontrib>LI, Hong-jin</creatorcontrib><creatorcontrib>NAKATANI, Yumi</creatorcontrib><creatorcontrib>OZAKI, Motoaki</creatorcontrib><creatorcontrib>KOSAKA, Maki</creatorcontrib><creatorcontrib>ISHII, Norihisa</creatorcontrib><creatorcontrib>NISHIMURA, Hiroyuki</creatorcontrib><creatorcontrib>FURUKAWA, Fukumi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>JAPANESE JOURNAL OF LEPROSY</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KANAZAWA, Nobuo</au><au>MIKITA, Naoya</au><au>LI, Hong-jin</au><au>NAKATANI, Yumi</au><au>OZAKI, Motoaki</au><au>KOSAKA, Maki</au><au>ISHII, Norihisa</au><au>NISHIMURA, Hiroyuki</au><au>FURUKAWA, Fukumi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic involvement of bacterial sensor molecules in Japanese leprosy</atitle><jtitle>JAPANESE JOURNAL OF LEPROSY</jtitle><addtitle>Jpn J Lepr</addtitle><date>2009-09</date><risdate>2009</risdate><volume>78</volume><issue>3</issue><spage>255</spage><epage>261</epage><pages>255-261</pages><issn>1342-3681</issn><eissn>1884-314X</eissn><abstract>Occurrence of new patients of leprosy, caused by Mycobacterium leprae infection, is now almost absent in Japan but is still uncontrolled in developing countries. As one factor affecting the disease development, genetic predisposition of a host has been considered to be associated. Actually, various gene mutations have been reported to be associated at two stages of the disease progression, not only establishment of the disease but also determination of the phenotype, such as lepromatous (L)-type, tuberculoid (T)-type and reversal reaction. On the basis of recent progress of the research on innate immunity, here we analyzed single nucleotide polymorphisms (SNPs) of the genes of major bacterial sensor molecules expressed in antigen-presenting cells, TLR2 , DC-SIGN , NOD1 and NOD2 , in Japanese leprosy patients. As a result, frequency of polymorphisms in DC-SIGN -336 showed significant difference between the leprosy patients and the healthy controls, reflecting its role in establishment of the disease. 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subjects | Antigen-Presenting Cells - immunology Asian Continental Ancestry Group bacterial sensor molecule Cell Adhesion Molecules - genetics gene polymorphism Genetic Predisposition to Disease - genetics Genotype Humans Immunity, Innate - genetics Japanese Lectins, C-Type - genetics leprosy Nod1 Signaling Adaptor Protein - genetics Nod2 Signaling Adaptor Protein - genetics Polymorphism, Single Nucleotide - genetics Receptors, Cell Surface - genetics Toll-Like Receptor 2 - genetics |
title | Genetic involvement of bacterial sensor molecules in Japanese leprosy |
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