Identification of new SLE-associated genes with a two-step Bayesian study design
Identifieur interne : 000A82 ( Ncbi/Merge ); précédent : 000A81; suivant : 000A83Identification of new SLE-associated genes with a two-step Bayesian study design
Auteurs : D L Armstrong ; A. Reiff ; B L. Myones ; F P. Quismorio ; M. Klein-Gitelman ; D. Mccurdy ; L. Wagner-Weiner ; E. Silverman ; J O Ojwang ; K M Kaufman ; J A Kelly ; J T Merrill ; J B Harley ; S-C Bae ; T J Vyse ; G S Gilkeson ; P M Gaffney ; K L Moser ; C. Putterman ; J C Edberg ; E E Brown ; J. Ziegler ; C D Langefeld ; R. Zidovetzki ; C O JacobSource :
- Genes and immunity [ 1466-4879 ] ; 2009.
Abstract
In our previous study, we utilized a Bayesian design to probe the association of ~1,000 genes (~10,000 SNPs) with SLE on a moderate number of trios of parents and children with SLE. Two genes associated with SLE with a multitest corrected False Discovery Rate (FDR) of <0.05. were identified, and a number of noteworthy genes with FDR of <0.8 were also found, pointing out a future direction for the study. In the present report, using a large population of controls and adult- or -childhood onset SLE cases, we have extended the previous investigation to explore the SLE association of ten of these noteworthy genes (109 SNPs). We have found that seven of these genes exhibit significant (FDR < 0.05) association with SLE, both confirming some genes that have previously been found to be associated with SLE (PTPN22 and IRF5) and novel findings of genes (KLRG1, IL-16, PTPRT, TLR8 and CASP10) which have not been previously reported. The results signify that the two-step candidate pathway design is an efficient way to study the genetic foundations of complex diseases. Furthermore, the novel genes identified in this study point to new directions in both the diagnosis and the eventual treatment of this debilitating disease.
Url:
DOI: 10.1038/gene.2009.38
PubMed: 19440200
PubMed Central: 3434884
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Putterman</name><affiliation><nlm:aff>NONE</nlm:aff></affiliation></author><author><name sortKey="Edberg, J C" sort="Edberg, J C" uniqKey="Edberg J" first="J C" last="Edberg">J C Edberg</name><affiliation><nlm:aff>NONE</nlm:aff></affiliation></author><author><name sortKey="Brown, E E" sort="Brown, E E" uniqKey="Brown E" first="E E" last="Brown">E E Brown</name><affiliation><nlm:aff>NONE</nlm:aff></affiliation></author><author><name sortKey="Ziegler, J" sort="Ziegler, J" uniqKey="Ziegler J" first="J" last="Ziegler">J. Ziegler</name><affiliation><nlm:aff>NONE</nlm:aff></affiliation></author><author><name sortKey="Langefeld, C D" sort="Langefeld, C D" uniqKey="Langefeld C" first="C D" last="Langefeld">C D Langefeld</name><affiliation><nlm:aff>NONE</nlm:aff></affiliation></author><author><name sortKey="Zidovetzki, R" sort="Zidovetzki, R" uniqKey="Zidovetzki R" first="R" last="Zidovetzki">R. Zidovetzki</name><affiliation><nlm:aff>NONE</nlm:aff></affiliation></author><author><name sortKey="Jacob, C O" sort="Jacob, C O" uniqKey="Jacob C" first="C O" last="Jacob">C O Jacob</name><affiliation><nlm:aff>NONE</nlm:aff></affiliation></author></analytic><series><title level="j">Genes and immunity</title><idno type="ISSN">1466-4879</idno><idno type="eISSN">1476-5470</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">In our previous study, we utilized a Bayesian design to probe the association of ~1,000 genes (~10,000 SNPs) with SLE on a moderate number of trios of parents and children with SLE. Two genes associated with SLE with a multitest corrected False Discovery Rate (FDR) of <0.05. were identified, and a number of noteworthy genes with FDR of <0.8 were also found, pointing out a future direction for the study. In the present report, using a large population of controls and adult- or -childhood onset SLE cases, we have extended the previous investigation to explore the SLE association of ten of these noteworthy genes (109 SNPs). We have found that seven of these genes exhibit significant (FDR < 0.05) association with SLE, both confirming some genes that have previously been found to be associated with SLE (PTPN22 and IRF5) and novel findings of genes (KLRG1, IL-16, PTPRT, TLR8 and CASP10) which have not been previously reported. The results signify that the two-step candidate pathway design is an efficient way to study the genetic foundations of complex diseases. Furthermore, the novel genes identified in this study point to new directions in both the diagnosis and the eventual treatment of this debilitating disease.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">100953417</journal-id><journal-id journal-id-type="pubmed-jr-id">21482</journal-id><journal-id journal-id-type="nlm-ta">Genes Immun</journal-id><journal-id journal-id-type="iso-abbrev">Genes Immun.</journal-id><journal-title-group><journal-title>Genes and immunity</journal-title></journal-title-group><issn pub-type="ppub">1466-4879</issn><issn pub-type="epub">1476-5470</issn></journal-meta><article-meta><article-id pub-id-type="pmid">19440200</article-id><article-id pub-id-type="pmc">3434884</article-id><article-id pub-id-type="doi">10.1038/gene.2009.38</article-id><article-id pub-id-type="manuscript">NIHMS358668</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Identification of new SLE-associated genes with a two-step Bayesian study design</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Armstrong</surname><given-names>D L</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Reiff</surname><given-names>A</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Myones</surname><given-names>B L.</given-names></name><xref ref-type="aff" rid="A4">4</xref></contrib><contrib contrib-type="author"><name><surname>Quismorio</surname><given-names>F P.</given-names><suffix>Jr</suffix></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Klein-Gitelman</surname><given-names>M</given-names></name><xref ref-type="aff" rid="A5">5</xref></contrib><contrib contrib-type="author"><name><surname>McCurdy</surname><given-names>D</given-names></name><xref ref-type="aff" rid="A6">6</xref></contrib><contrib contrib-type="author"><name><surname>Wagner-Weiner</surname><given-names>L</given-names></name><xref ref-type="aff" rid="A7">7</xref></contrib><contrib contrib-type="author"><name><surname>Silverman</surname><given-names>E</given-names></name><xref ref-type="aff" rid="A8">8</xref></contrib><contrib contrib-type="author"><name><surname>Ojwang</surname><given-names>J O</given-names></name><xref ref-type="aff" rid="A9">9</xref></contrib><contrib contrib-type="author"><name><surname>Kaufman</surname><given-names>K M</given-names></name><xref ref-type="aff" rid="A9">9</xref></contrib><contrib contrib-type="author"><name><surname>Kelly</surname><given-names>J A</given-names></name><xref ref-type="aff" rid="A9">9</xref></contrib><contrib contrib-type="author"><name><surname>Merrill</surname><given-names>J T</given-names></name><xref ref-type="aff" rid="A9">9</xref></contrib><contrib contrib-type="author"><name><surname>Harley</surname><given-names>J B</given-names></name><xref ref-type="aff" rid="A9">9</xref></contrib><contrib contrib-type="author"><name><surname>Bae</surname><given-names>S-C</given-names></name><xref ref-type="aff" rid="A10">10</xref></contrib><contrib contrib-type="author"><name><surname>Vyse</surname><given-names>T J</given-names></name><xref ref-type="aff" rid="A11">11</xref></contrib><contrib contrib-type="author"><name><surname>Gilkeson</surname><given-names>G S</given-names></name><xref ref-type="aff" rid="A12">12</xref></contrib><contrib contrib-type="author"><name><surname>Gaffney</surname><given-names>P M</given-names></name><xref ref-type="aff" rid="A9">9</xref></contrib><contrib contrib-type="author"><name><surname>Moser</surname><given-names>K L</given-names></name><xref ref-type="aff" rid="A9">9</xref></contrib><contrib contrib-type="author"><name><surname>Putterman</surname><given-names>C</given-names></name><xref ref-type="aff" rid="A13">13</xref></contrib><contrib contrib-type="author"><name><surname>Edberg</surname><given-names>J C</given-names></name><xref ref-type="aff" rid="A14">14</xref></contrib><contrib contrib-type="author"><name><surname>Brown</surname><given-names>E E</given-names></name><xref ref-type="aff" rid="A14">14</xref></contrib><contrib contrib-type="author"><name><surname>Ziegler</surname><given-names>J</given-names></name><xref ref-type="aff" rid="A15">15</xref></contrib><contrib contrib-type="author"><name><surname>Langefeld</surname><given-names>C D</given-names></name><xref ref-type="aff" rid="A15">15</xref></contrib><contrib contrib-type="author"><name><surname>Zidovetzki</surname><given-names>R</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Jacob</surname><given-names>C O</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1)</label>The Lupus Genetic Group, Department of Medicine, University of Southern California, Los Angeles, CA</aff><aff id="A2"><label>2)</label>Department of Cell Biology and Neuroscience, University of California, Riverside CA</aff><aff id="A3"><label>3)</label>Childrens Hospital of Los Angeles, Los Angeles, CA</aff><aff id="A4"><label>4)</label>Texas Children’s Hospital, Baylor College of Medicine, Houston, TX</aff><aff id="A5"><label>5)</label>Children’s Memorial Hospital and Northwestern University, Chicago IL</aff><aff id="A6"><label>6)</label>Department of Pediatrics, UCLA, Los Angeles CA</aff><aff id="A7"><label>7)</label>LaRabida Hospital and University of Chicago, Chicago, IL</aff><aff id="A8"><label>8)</label>Hospital for Sick Children, Toronto, OT, Canada</aff><aff id="A9"><label>9)</label>Oklahoma Medical Research Foundation, Oklahoma City, OK</aff><aff id="A10"><label>10)</label>Department of Rheumatology, the Hospital for Rheumatic Diseases, Hanyang University, Seoul, Republic of Korea</aff><aff id="A11"><label>11)</label>Imperial College London, Hammersmith Hospital, London UK</aff><aff id="A12"><label>12)</label>Medical University of South Carolina, Charleston, SC</aff><aff id="A13"><label>13)</label>Division of Rheumatology, Albert Einstein College of Medicine, Bronx, NY</aff><aff id="A14"><label>14)</label>Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, AL</aff><aff id="A15"><label>15)</label>Wake Forest University Health Sciences, Winston-Salem, NC</aff><pub-date pub-type="nihms-submitted"><day>4</day><month>3</month><year>2012</year></pub-date><pub-date pub-type="epub"><day>14</day><month>5</month><year>2009</year></pub-date><pub-date pub-type="ppub"><month>7</month><year>2009</year></pub-date><pub-date pub-type="pmc-release"><day>06</day><month>9</month><year>2012</year></pub-date><volume>10</volume><issue>5</issue><fpage>446</fpage><lpage>456</lpage><abstract><p id="P1">In our previous study, we utilized a Bayesian design to probe the association of ~1,000 genes (~10,000 SNPs) with SLE on a moderate number of trios of parents and children with SLE. Two genes associated with SLE with a multitest corrected False Discovery Rate (FDR) of <0.05. were identified, and a number of noteworthy genes with FDR of <0.8 were also found, pointing out a future direction for the study. In the present report, using a large population of controls and adult- or -childhood onset SLE cases, we have extended the previous investigation to explore the SLE association of ten of these noteworthy genes (109 SNPs). We have found that seven of these genes exhibit significant (FDR < 0.05) association with SLE, both confirming some genes that have previously been found to be associated with SLE (PTPN22 and IRF5) and novel findings of genes (KLRG1, IL-16, PTPRT, TLR8 and CASP10) which have not been previously reported. The results signify that the two-step candidate pathway design is an efficient way to study the genetic foundations of complex diseases. Furthermore, the novel genes identified in this study point to new directions in both the diagnosis and the eventual treatment of this debilitating disease.</p></abstract><kwd-group><kwd>Autoimmune disease</kwd><kwd>Genetic Association</kwd><kwd>KLRG1</kwd><kwd>IL-16</kwd><kwd>PTPRT</kwd><kwd>TLR8</kwd><kwd>CASP10</kwd><kwd>SNP</kwd></kwd-group><funding-group><award-group><funding-source country="United States">National Institute of Arthritis and Musculoskeletal and Skin Diseases : NIAMS</funding-source><award-id>R01 AR045650-05 || AR</award-id></award-group><award-group><funding-source country="United States">National Institute of Arthritis and Musculoskeletal and Skin Diseases : NIAMS</funding-source><award-id>R01 AR042460-07 || AR</award-id></award-group><award-group><funding-source country="United States">National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID</funding-source><award-id>R01 AI063622-02 || AI</award-id></award-group><award-group><funding-source country="United States">National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID</funding-source><award-id>R01 AI024717-13 || AI</award-id></award-group><award-group><funding-source country="United States">National Institute of Arthritis and Musculoskeletal and Skin Diseases : NIAMS</funding-source><award-id>P60 AR048095-01 || AR</award-id></award-group><award-group><funding-source country="United States">National Institute of Arthritis and Musculoskeletal and Skin Diseases : NIAMS</funding-source><award-id>P50 AR048940-01 || AR</award-id></award-group><award-group><funding-source country="United States">National Institute of Arthritis and Musculoskeletal and Skin Diseases : NIAMS</funding-source><award-id>P30 AR053483-02 || AR</award-id></award-group><award-group><funding-source country="United States">National Center for Research Resources : NCRR</funding-source><award-id>P20 RR020143-07 || RR</award-id></award-group><award-group><funding-source country="United States">National Institute of Arthritis and Musculoskeletal and Skin Diseases : NIAMS</funding-source><award-id>P01 AR049084-01 || AR</award-id></award-group></funding-group></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Armstrong, D L" sort="Armstrong, D L" uniqKey="Armstrong D" first="D L" last="Armstrong">D L Armstrong</name><name sortKey="Bae, S C" sort="Bae, S C" uniqKey="Bae S" first="S-C" last="Bae">S-C Bae</name><name sortKey="Brown, E E" sort="Brown, E E" uniqKey="Brown E" first="E E" last="Brown">E E Brown</name><name sortKey="Edberg, J C" sort="Edberg, J C" uniqKey="Edberg J" first="J C" last="Edberg">J C Edberg</name><name sortKey="Gaffney, P M" sort="Gaffney, P M" uniqKey="Gaffney P" first="P M" last="Gaffney">P M Gaffney</name><name sortKey="Gilkeson, G S" sort="Gilkeson, G S" uniqKey="Gilkeson G" first="G S" last="Gilkeson">G S Gilkeson</name><name sortKey="Harley, J B" sort="Harley, J B" uniqKey="Harley J" first="J B" last="Harley">J B Harley</name><name sortKey="Jacob, C O" sort="Jacob, C O" uniqKey="Jacob C" first="C O" last="Jacob">C O Jacob</name><name sortKey="Kaufman, K M" sort="Kaufman, K M" uniqKey="Kaufman K" first="K M" last="Kaufman">K M Kaufman</name><name sortKey="Kelly, J A" sort="Kelly, J A" uniqKey="Kelly J" first="J A" last="Kelly">J A Kelly</name><name sortKey="Klein Gitelman, M" sort="Klein Gitelman, M" uniqKey="Klein Gitelman M" first="M" last="Klein-Gitelman">M. Klein-Gitelman</name><name sortKey="Langefeld, C D" sort="Langefeld, C D" uniqKey="Langefeld C" first="C D" last="Langefeld">C D Langefeld</name><name sortKey="Mccurdy, D" sort="Mccurdy, D" uniqKey="Mccurdy D" first="D" last="Mccurdy">D. Mccurdy</name><name sortKey="Merrill, J T" sort="Merrill, J T" uniqKey="Merrill J" first="J T" last="Merrill">J T Merrill</name><name sortKey="Moser, K L" sort="Moser, K L" uniqKey="Moser K" first="K L" last="Moser">K L Moser</name><name sortKey="Myones, B L" sort="Myones, B L" uniqKey="Myones B" first="B L." last="Myones">B L. Myones</name><name sortKey="Ojwang, J O" sort="Ojwang, J O" uniqKey="Ojwang J" first="J O" last="Ojwang">J O Ojwang</name><name sortKey="Putterman, C" sort="Putterman, C" uniqKey="Putterman C" first="C" last="Putterman">C. Putterman</name><name sortKey="Quismorio, F P" sort="Quismorio, F P" uniqKey="Quismorio F" first="F P." last="Quismorio">F P. Quismorio</name><name sortKey="Reiff, A" sort="Reiff, A" uniqKey="Reiff A" first="A" last="Reiff">A. Reiff</name><name sortKey="Silverman, E" sort="Silverman, E" uniqKey="Silverman E" first="E" last="Silverman">E. Silverman</name><name sortKey="Vyse, T J" sort="Vyse, T J" uniqKey="Vyse T" first="T J" last="Vyse">T J Vyse</name><name sortKey="Wagner Weiner, L" sort="Wagner Weiner, L" uniqKey="Wagner Weiner L" first="L" last="Wagner-Weiner">L. Wagner-Weiner</name><name sortKey="Zidovetzki, R" sort="Zidovetzki, R" uniqKey="Zidovetzki R" first="R" last="Zidovetzki">R. Zidovetzki</name><name sortKey="Ziegler, J" sort="Ziegler, J" uniqKey="Ziegler J" first="J" last="Ziegler">J. Ziegler</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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