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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The <italic>iddm4</italic> Locus Segregates With Diabetes Susceptibility in Congenic WF.<italic>iddm4</italic> Rats</title><author><name sortKey="Mordes, John P" sort="Mordes, John P" uniqKey="Mordes J" first="John P." last="Mordes">John P. Mordes</name><affiliation><nlm:aff id="A1">Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts</nlm:aff></affiliation></author><author><name sortKey="Leif, Jean" sort="Leif, Jean" uniqKey="Leif J" first="Jean" last="Leif">Jean Leif</name><affiliation><nlm:aff id="A1">Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts</nlm:aff></affiliation></author><author><name sortKey="Novak, Stephen" sort="Novak, Stephen" uniqKey="Novak S" first="Stephen" last="Novak">Stephen Novak</name><affiliation><nlm:aff id="A2">Department of Microbiology and Immunology, MCP Hahnemann University, Philadelphia, Pennsylvania.</nlm:aff></affiliation></author><author><name sortKey="Descipio, Cheryl" sort="Descipio, Cheryl" uniqKey="Descipio C" first="Cheryl" last="Descipio">Cheryl Descipio</name><affiliation><nlm:aff id="A2">Department of Microbiology and Immunology, MCP Hahnemann University, Philadelphia, Pennsylvania.</nlm:aff></affiliation></author><author><name sortKey="Greiner, Dale L" sort="Greiner, Dale L" uniqKey="Greiner D" first="Dale L." last="Greiner">Dale L. Greiner</name><affiliation><nlm:aff id="A1">Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts</nlm:aff></affiliation></author><author><name sortKey="Blankenhorn, Elizabeth P" sort="Blankenhorn, Elizabeth P" uniqKey="Blankenhorn E" first="Elizabeth P." last="Blankenhorn">Elizabeth P. Blankenhorn</name><affiliation><nlm:aff id="A2">Department of Microbiology and Immunology, MCP Hahnemann University, Philadelphia, Pennsylvania.</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">12401717</idno><idno type="pmc">4034451</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4034451</idno><idno type="RBID">PMC:4034451</idno><date when="2002">2002</date><idno type="wicri:Area/Pmc/Corpus">000752</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000752</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The <italic>iddm4</italic> Locus Segregates With Diabetes Susceptibility in Congenic WF.<italic>iddm4</italic> Rats</title><author><name sortKey="Mordes, John P" sort="Mordes, John P" uniqKey="Mordes J" first="John P." last="Mordes">John P. Mordes</name><affiliation><nlm:aff id="A1">Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts</nlm:aff></affiliation></author><author><name sortKey="Leif, Jean" sort="Leif, Jean" uniqKey="Leif J" first="Jean" last="Leif">Jean Leif</name><affiliation><nlm:aff id="A1">Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts</nlm:aff></affiliation></author><author><name sortKey="Novak, Stephen" sort="Novak, Stephen" uniqKey="Novak S" first="Stephen" last="Novak">Stephen Novak</name><affiliation><nlm:aff id="A2">Department of Microbiology and Immunology, MCP Hahnemann University, Philadelphia, Pennsylvania.</nlm:aff></affiliation></author><author><name sortKey="Descipio, Cheryl" sort="Descipio, Cheryl" uniqKey="Descipio C" first="Cheryl" last="Descipio">Cheryl Descipio</name><affiliation><nlm:aff id="A2">Department of Microbiology and Immunology, MCP Hahnemann University, Philadelphia, Pennsylvania.</nlm:aff></affiliation></author><author><name sortKey="Greiner, Dale L" sort="Greiner, Dale L" uniqKey="Greiner D" first="Dale L." last="Greiner">Dale L. Greiner</name><affiliation><nlm:aff id="A1">Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts</nlm:aff></affiliation></author><author><name sortKey="Blankenhorn, Elizabeth P" sort="Blankenhorn, Elizabeth P" uniqKey="Blankenhorn E" first="Elizabeth P." last="Blankenhorn">Elizabeth P. Blankenhorn</name><affiliation><nlm:aff id="A2">Department of Microbiology and Immunology, MCP Hahnemann University, Philadelphia, Pennsylvania.</nlm:aff></affiliation></author></analytic><series><title level="j">Diabetes</title><idno type="ISSN">0012-1797</idno><idno type="eISSN">1939-327X</idno><imprint><date when="2002">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Viral antibody–free BBDR and WF rats never develop spontaneous diabetes. BBDR rats, however, develop autoimmune diabetes after perturbation of the immune system, e.g., by viral infection. We previously identified a disease-susceptibility locus in the BBDR rat, <italic>iddm4</italic>, which is associated with the development of autoimmune diabetes after treatment with polyinosinic:polycytidylic acid and an antibody that depletes ART2<sup>+</sup> regulatory cells. We have now developed lines of congenic WF.<italic>iddm4</italic> rats and report that in an intercross of N5 generation WF.<italic>iddm4</italic> rats, ∼70% of animals either homozygous or heterozygous for the BBDR origin allele of <italic>iddm4</italic> became hyperglycemic after treatment to induce diabetes. Fewer than 20% of rats expressing the WF origin allele of <italic>iddm4</italic> became diabetic. Testing the progeny of various recombinant N5 WF.<italic>iddm4</italic> congenic rats for susceptibility to diabetes suggests that <italic>iddm4</italic> is centered on a small segment of chromosome 4 bounded by the proximal marker <italic>D4Rat135</italic> and the distal marker <italic>D4Got51</italic>, an interval of <2.8 cM. The allele at <italic>iddm4</italic> has 79% sensitivity and 80% specificity in prediction of diabetes in rats that are segregating for this locus. These characteristics suggest that <italic>iddm4</italic> is one of the most powerful non–major histocompatibility complex determinants of susceptibility to autoimmune diabetes described to date.</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">0372763</journal-id><journal-id journal-id-type="pubmed-jr-id">3397</journal-id><journal-id journal-id-type="nlm-ta">Diabetes</journal-id><journal-id journal-id-type="iso-abbrev">Diabetes</journal-id><journal-title-group><journal-title>Diabetes</journal-title></journal-title-group><issn pub-type="ppub">0012-1797</issn><issn pub-type="epub">1939-327X</issn></journal-meta><article-meta><article-id pub-id-type="pmid">12401717</article-id><article-id pub-id-type="pmc">4034451</article-id><article-id pub-id-type="manuscript">NIHMS565755</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>The <italic>iddm4</italic> Locus Segregates With Diabetes Susceptibility in Congenic WF.<italic>iddm4</italic> Rats</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Mordes</surname><given-names>John P.</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Leif</surname><given-names>Jean</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Novak</surname><given-names>Stephen</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>DeScipio</surname><given-names>Cheryl</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Greiner</surname><given-names>Dale L.</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Blankenhorn</surname><given-names>Elizabeth P.</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib></contrib-group><aff id="A1"><label>1</label>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts</aff><aff id="A2"><label>2</label>Department of Microbiology and Immunology, MCP Hahnemann University, Philadelphia, Pennsylvania.</aff><author-notes><corresp id="CR1">Address correspondence and reprint requests to Dr. John Mordes, Diabetes Division, 373 Plantation St., Biotech 2, Suite 218, Worcester, MA 01605. <email>john.mordes@umassmed.edu</email>.</corresp></author-notes><pub-date pub-type="nihms-submitted"><day>14</day><month>4</month><year>2014</year></pub-date><pub-date pub-type="ppub"><month>11</month><year>2002</year></pub-date><pub-date pub-type="pmc-release"><day>27</day><month>5</month><year>2014</year></pub-date><volume>51</volume><issue>11</issue><fpage>3254</fpage><lpage>3262</lpage><abstract><p id="P1">Viral antibody–free BBDR and WF rats never develop spontaneous diabetes. BBDR rats, however, develop autoimmune diabetes after perturbation of the immune system, e.g., by viral infection. We previously identified a disease-susceptibility locus in the BBDR rat, <italic>iddm4</italic>, which is associated with the development of autoimmune diabetes after treatment with polyinosinic:polycytidylic acid and an antibody that depletes ART2<sup>+</sup> regulatory cells. We have now developed lines of congenic WF.<italic>iddm4</italic> rats and report that in an intercross of N5 generation WF.<italic>iddm4</italic> rats, ∼70% of animals either homozygous or heterozygous for the BBDR origin allele of <italic>iddm4</italic> became hyperglycemic after treatment to induce diabetes. Fewer than 20% of rats expressing the WF origin allele of <italic>iddm4</italic> became diabetic. Testing the progeny of various recombinant N5 WF.<italic>iddm4</italic> congenic rats for susceptibility to diabetes suggests that <italic>iddm4</italic> is centered on a small segment of chromosome 4 bounded by the proximal marker <italic>D4Rat135</italic> and the distal marker <italic>D4Got51</italic>, an interval of <2.8 cM. The allele at <italic>iddm4</italic> has 79% sensitivity and 80% specificity in prediction of diabetes in rats that are segregating for this locus. These characteristics suggest that <italic>iddm4</italic> is one of the most powerful non–major histocompatibility complex determinants of susceptibility to autoimmune diabetes described to date.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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