Interleukin-10, Polymorphism in SLC11A1 (formerly NRAMP1), and Susceptibility to Tuberculosis
Host genetic factors are major determinants of susceptibility to tuberculosis, and an understanding of the molecular basis of this observation has major implications for the development of novel therapies and vaccines. Slc11a1 (formerly Nramp1), the first murine infection susceptibility locus identi...
Gespeichert in:
| Veröffentlicht in: | The Journal of infectious diseases 2002-12, Vol.186 (12), p.1808-1814 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1814 |
|---|---|
| container_issue | 12 |
| container_start_page | 1808 |
| container_title | The Journal of infectious diseases |
| container_volume | 186 |
| creator | Awomoyi, Agnes A. Marchant, Arnaud Howson, Joanna M. M. McAdam, Keith P. W. J. Blackwell, Jenefer M. Newport, Melanie J. |
| description | Host genetic factors are major determinants of susceptibility to tuberculosis, and an understanding of the molecular basis of this observation has major implications for the development of novel therapies and vaccines. Slc11a1 (formerly Nramp1), the first murine infection susceptibility locus identified, regulates early innate responses to intracellular pathogens. Variation in the human homologue SLC11A1 is associated with and linked to tuberculosis in genetically different populations. In a case-control study of 329 tuberculosis case patients and 324 control subjects, the association between allele 2 of a functional SLC11A1 polymorphism and tuberculosis has been reproduced. This variant is associated with higher lipopolysaccharide-induced production of the macrophage-deactivating cytokine interleukin-10. Furthermore, monocytes from persons who develop tuberculosis innately produce more interleukin-10 than do monocytes from healthy control subjects. These data therefore confirm the importance of SLC11A1 in tuberculosis susceptibility in humans and suggest that SLC11A1 influences tuberculosis susceptibility by regulation of interleukin-10 |
| doi_str_mv | 10.1086/345920 |
| format | Article |
| fullrecord | <record><control><sourceid>jstor_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_72712539</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><jstor_id>30077982</jstor_id><oup_id>10.1086/345920</oup_id><sourcerecordid>30077982</sourcerecordid><originalsourceid>FETCH-LOGICAL-c449t-a9431847b196abf0662398507d8f712d0a4e0399f73da30822b7d4ed5e44c8503</originalsourceid><addsrcrecordid>eNqF0WuL1DAUBuAgijuu-g-UKqwobPXk0lw-DsPeYNTVHUEECWmbYmbbpiYtOP_eSIcdEMRP-XAe3pzDi9BTDG8xSP6OskIRuIcWuKAi5xzT-2gBQEiOpVJH6FGMWwBglIuH6AgTxoTgYoG-X_WjDa2dbl2fYzjNrn2763wYfrjYZa7PbtYrjJc4e9340CW5yz58Xr6_xm9OM9PX2c0UKzuMrnStG3fZ6LPNVNpQTa2PLj5GDxrTRvtk_x6jL-dnm9Vlvv54cbVarvOKMTXmRjGKJRMlVtyUDXBOqJIFiFo2ApMaDLNAlWoErQ0FSUgpambrwjJWJUeP0as5dwj-52TjqDuX9mpb01s_RS1Iiimo-i_EUhRSgEjw5V9w66fQpyM0IVSqQlB5SKuCjzHYRg_BdSbsNAb9pxY915Lg833aVHa2PrB9Dwmc7IGJlWmbYPrKxYNj6XrKi-RezM5Pw78_ezabbRx9uFMUQAglSZrn89zF0f66m5twq9MmotCXX7_p8w2_IJ_oRgP9DfH0spk</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>223895738</pqid></control><display><type>article</type><title>Interleukin-10, Polymorphism in SLC11A1 (formerly NRAMP1), and Susceptibility to Tuberculosis</title><source>JSTOR Archive Collection A-Z Listing</source><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Awomoyi, Agnes A. ; Marchant, Arnaud ; Howson, Joanna M. M. ; McAdam, Keith P. W. J. ; Blackwell, Jenefer M. ; Newport, Melanie J.</creator><creatorcontrib>Awomoyi, Agnes A. ; Marchant, Arnaud ; Howson, Joanna M. M. ; McAdam, Keith P. W. J. ; Blackwell, Jenefer M. ; Newport, Melanie J.</creatorcontrib><description>Host genetic factors are major determinants of susceptibility to tuberculosis, and an understanding of the molecular basis of this observation has major implications for the development of novel therapies and vaccines. Slc11a1 (formerly Nramp1), the first murine infection susceptibility locus identified, regulates early innate responses to intracellular pathogens. Variation in the human homologue SLC11A1 is associated with and linked to tuberculosis in genetically different populations. In a case-control study of 329 tuberculosis case patients and 324 control subjects, the association between allele 2 of a functional SLC11A1 polymorphism and tuberculosis has been reproduced. This variant is associated with higher lipopolysaccharide-induced production of the macrophage-deactivating cytokine interleukin-10. Furthermore, monocytes from persons who develop tuberculosis innately produce more interleukin-10 than do monocytes from healthy control subjects. These data therefore confirm the importance of SLC11A1 in tuberculosis susceptibility in humans and suggest that SLC11A1 influences tuberculosis susceptibility by regulation of interleukin-10</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1086/345920</identifier><identifier>PMID: 12447767</identifier><identifier>CODEN: JIDIAQ</identifier><language>eng</language><publisher>Chicago, IL: The University of Chicago Press</publisher><subject>Adult ; Alleles ; Bacterial diseases ; Biological and medical sciences ; Case-Control Studies ; Cation Transport Proteins - genetics ; Cytokines ; Gambia ; Genetic Predisposition to Disease ; Genotype ; Genotypes ; Human bacterial diseases ; Humans ; Immunity, Innate ; Infections ; Infectious diseases ; Interleukin-10 - biosynthesis ; Macrophages ; Major Article ; Male ; Medical genetics ; Medical sciences ; Mice ; Middle Aged ; Monocytes ; Monocytes - immunology ; Mycobacterium tuberculosis ; Polymorphism, Genetic ; Tuberculosis ; Tuberculosis and atypical mycobacterial infections ; Tuberculosis, Pulmonary - blood ; Tuberculosis, Pulmonary - genetics ; Tuberculosis, Pulmonary - immunology</subject><ispartof>The Journal of infectious diseases, 2002-12, Vol.186 (12), p.1808-1814</ispartof><rights>Copyright 2002 Infectious Diseases Society of America</rights><rights>2002 by the Infectious Diseases Society of America 2002</rights><rights>2003 INIST-CNRS</rights><rights>Copyright University of Chicago, acting through its Press Dec 15, 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-a9431847b196abf0662398507d8f712d0a4e0399f73da30822b7d4ed5e44c8503</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/30077982$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/30077982$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,27901,27902,57992,58225</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14399365$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12447767$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Awomoyi, Agnes A.</creatorcontrib><creatorcontrib>Marchant, Arnaud</creatorcontrib><creatorcontrib>Howson, Joanna M. M.</creatorcontrib><creatorcontrib>McAdam, Keith P. W. J.</creatorcontrib><creatorcontrib>Blackwell, Jenefer M.</creatorcontrib><creatorcontrib>Newport, Melanie J.</creatorcontrib><title>Interleukin-10, Polymorphism in SLC11A1 (formerly NRAMP1), and Susceptibility to Tuberculosis</title><title>The Journal of infectious diseases</title><addtitle>The Journal of Infectious Diseases</addtitle><addtitle>The Journal of Infectious Diseases</addtitle><description>Host genetic factors are major determinants of susceptibility to tuberculosis, and an understanding of the molecular basis of this observation has major implications for the development of novel therapies and vaccines. Slc11a1 (formerly Nramp1), the first murine infection susceptibility locus identified, regulates early innate responses to intracellular pathogens. Variation in the human homologue SLC11A1 is associated with and linked to tuberculosis in genetically different populations. In a case-control study of 329 tuberculosis case patients and 324 control subjects, the association between allele 2 of a functional SLC11A1 polymorphism and tuberculosis has been reproduced. This variant is associated with higher lipopolysaccharide-induced production of the macrophage-deactivating cytokine interleukin-10. Furthermore, monocytes from persons who develop tuberculosis innately produce more interleukin-10 than do monocytes from healthy control subjects. These data therefore confirm the importance of SLC11A1 in tuberculosis susceptibility in humans and suggest that SLC11A1 influences tuberculosis susceptibility by regulation of interleukin-10</description><subject>Adult</subject><subject>Alleles</subject><subject>Bacterial diseases</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Cation Transport Proteins - genetics</subject><subject>Cytokines</subject><subject>Gambia</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Genotypes</subject><subject>Human bacterial diseases</subject><subject>Humans</subject><subject>Immunity, Innate</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Interleukin-10 - biosynthesis</subject><subject>Macrophages</subject><subject>Major Article</subject><subject>Male</subject><subject>Medical genetics</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Middle Aged</subject><subject>Monocytes</subject><subject>Monocytes - immunology</subject><subject>Mycobacterium tuberculosis</subject><subject>Polymorphism, Genetic</subject><subject>Tuberculosis</subject><subject>Tuberculosis and atypical mycobacterial infections</subject><subject>Tuberculosis, Pulmonary - blood</subject><subject>Tuberculosis, Pulmonary - genetics</subject><subject>Tuberculosis, Pulmonary - immunology</subject><issn>0022-1899</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0WuL1DAUBuAgijuu-g-UKqwobPXk0lw-DsPeYNTVHUEECWmbYmbbpiYtOP_eSIcdEMRP-XAe3pzDi9BTDG8xSP6OskIRuIcWuKAi5xzT-2gBQEiOpVJH6FGMWwBglIuH6AgTxoTgYoG-X_WjDa2dbl2fYzjNrn2763wYfrjYZa7PbtYrjJc4e9340CW5yz58Xr6_xm9OM9PX2c0UKzuMrnStG3fZ6LPNVNpQTa2PLj5GDxrTRvtk_x6jL-dnm9Vlvv54cbVarvOKMTXmRjGKJRMlVtyUDXBOqJIFiFo2ApMaDLNAlWoErQ0FSUgpambrwjJWJUeP0as5dwj-52TjqDuX9mpb01s_RS1Iiimo-i_EUhRSgEjw5V9w66fQpyM0IVSqQlB5SKuCjzHYRg_BdSbsNAb9pxY915Lg833aVHa2PrB9Dwmc7IGJlWmbYPrKxYNj6XrKi-RezM5Pw78_ezabbRx9uFMUQAglSZrn89zF0f66m5twq9MmotCXX7_p8w2_IJ_oRgP9DfH0spk</recordid><startdate>20021215</startdate><enddate>20021215</enddate><creator>Awomoyi, Agnes A.</creator><creator>Marchant, Arnaud</creator><creator>Howson, Joanna M. M.</creator><creator>McAdam, Keith P. W. J.</creator><creator>Blackwell, Jenefer M.</creator><creator>Newport, Melanie J.</creator><general>The University of Chicago Press</general><general>University of Chicago Press</general><general>Oxford University Press</general><scope>BSCLL</scope><scope>IQODW</scope><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>K9.</scope><scope>NAPCQ</scope><scope>7QL</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>20021215</creationdate><title>Interleukin-10, Polymorphism in SLC11A1 (formerly NRAMP1), and Susceptibility to Tuberculosis</title><author>Awomoyi, Agnes A. ; Marchant, Arnaud ; Howson, Joanna M. M. ; McAdam, Keith P. W. J. ; Blackwell, Jenefer M. ; Newport, Melanie J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-a9431847b196abf0662398507d8f712d0a4e0399f73da30822b7d4ed5e44c8503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adult</topic><topic>Alleles</topic><topic>Bacterial diseases</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Cation Transport Proteins - genetics</topic><topic>Cytokines</topic><topic>Gambia</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Genotypes</topic><topic>Human bacterial diseases</topic><topic>Humans</topic><topic>Immunity, Innate</topic><topic>Infections</topic><topic>Infectious diseases</topic><topic>Interleukin-10 - biosynthesis</topic><topic>Macrophages</topic><topic>Major Article</topic><topic>Male</topic><topic>Medical genetics</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Middle Aged</topic><topic>Monocytes</topic><topic>Monocytes - immunology</topic><topic>Mycobacterium tuberculosis</topic><topic>Polymorphism, Genetic</topic><topic>Tuberculosis</topic><topic>Tuberculosis and atypical mycobacterial infections</topic><topic>Tuberculosis, Pulmonary - blood</topic><topic>Tuberculosis, Pulmonary - genetics</topic><topic>Tuberculosis, Pulmonary - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Awomoyi, Agnes A.</creatorcontrib><creatorcontrib>Marchant, Arnaud</creatorcontrib><creatorcontrib>Howson, Joanna M. M.</creatorcontrib><creatorcontrib>McAdam, Keith P. W. J.</creatorcontrib><creatorcontrib>Blackwell, Jenefer M.</creatorcontrib><creatorcontrib>Newport, Melanie J.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Awomoyi, Agnes A.</au><au>Marchant, Arnaud</au><au>Howson, Joanna M. M.</au><au>McAdam, Keith P. W. J.</au><au>Blackwell, Jenefer M.</au><au>Newport, Melanie J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interleukin-10, Polymorphism in SLC11A1 (formerly NRAMP1), and Susceptibility to Tuberculosis</atitle><jtitle>The Journal of infectious diseases</jtitle><stitle>The Journal of Infectious Diseases</stitle><addtitle>The Journal of Infectious Diseases</addtitle><date>2002-12-15</date><risdate>2002</risdate><volume>186</volume><issue>12</issue><spage>1808</spage><epage>1814</epage><pages>1808-1814</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><coden>JIDIAQ</coden><abstract>Host genetic factors are major determinants of susceptibility to tuberculosis, and an understanding of the molecular basis of this observation has major implications for the development of novel therapies and vaccines. Slc11a1 (formerly Nramp1), the first murine infection susceptibility locus identified, regulates early innate responses to intracellular pathogens. Variation in the human homologue SLC11A1 is associated with and linked to tuberculosis in genetically different populations. In a case-control study of 329 tuberculosis case patients and 324 control subjects, the association between allele 2 of a functional SLC11A1 polymorphism and tuberculosis has been reproduced. This variant is associated with higher lipopolysaccharide-induced production of the macrophage-deactivating cytokine interleukin-10. Furthermore, monocytes from persons who develop tuberculosis innately produce more interleukin-10 than do monocytes from healthy control subjects. These data therefore confirm the importance of SLC11A1 in tuberculosis susceptibility in humans and suggest that SLC11A1 influences tuberculosis susceptibility by regulation of interleukin-10</abstract><cop>Chicago, IL</cop><pub>The University of Chicago Press</pub><pmid>12447767</pmid><doi>10.1086/345920</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0022-1899 |
| ispartof | The Journal of infectious diseases, 2002-12, Vol.186 (12), p.1808-1814 |
| issn | 0022-1899 1537-6613 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_72712539 |
| source | JSTOR Archive Collection A-Z Listing; Oxford University Press Journals All Titles (1996-Current); MEDLINE; Alma/SFX Local Collection |
| subjects | Adult Alleles Bacterial diseases Biological and medical sciences Case-Control Studies Cation Transport Proteins - genetics Cytokines Gambia Genetic Predisposition to Disease Genotype Genotypes Human bacterial diseases Humans Immunity, Innate Infections Infectious diseases Interleukin-10 - biosynthesis Macrophages Major Article Male Medical genetics Medical sciences Mice Middle Aged Monocytes Monocytes - immunology Mycobacterium tuberculosis Polymorphism, Genetic Tuberculosis Tuberculosis and atypical mycobacterial infections Tuberculosis, Pulmonary - blood Tuberculosis, Pulmonary - genetics Tuberculosis, Pulmonary - immunology |
| title | Interleukin-10, Polymorphism in SLC11A1 (formerly NRAMP1), and Susceptibility to Tuberculosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T04%3A19%3A12IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-jstor_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Interleukin-10,%20Polymorphism%20in%20SLC11A1%20(formerly%20NRAMP1),%20and%20Susceptibility%20to%20Tuberculosis&rft.jtitle=The%20Journal%20of%20infectious%20diseases&rft.au=Awomoyi,%20Agnes%20A.&rft.date=2002-12-15&rft.volume=186&rft.issue=12&rft.spage=1808&rft.epage=1814&rft.pages=1808-1814&rft.issn=0022-1899&rft.eissn=1537-6613&rft.coden=JIDIAQ&rft_id=info:doi/10.1086/345920&rft_dat=%3Cjstor_proqu%3E30077982%3C/jstor_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=223895738&rft_id=info:pmid/12447767&rft_jstor_id=30077982&rft_oup_id=10.1086/345920&rfr_iscdi=true |