The iddm4 Locus Segregates With Diabetes Susceptibility in Congenic WF.iddm4 Rats
Identifieur interne : 000494 ( Pmc/Curation ); précédent : 000493; suivant : 000495The iddm4 Locus Segregates With Diabetes Susceptibility in Congenic WF.iddm4 Rats
Auteurs : John P. Mordes [États-Unis] ; Jean Leif [États-Unis] ; Stephen Novak ; Cheryl Descipio ; Dale L. Greiner [États-Unis] ; Elizabeth P. BlankenhornSource :
- Diabetes [ 0012-1797 ] ; 2002.
Abstract
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,
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PubMed: 12401717
PubMed Central: 4034451
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Stephen Novak<affiliation><nlm:aff id="A2">Department of Microbiology and Immunology, MCP Hahnemann University, Philadelphia, Pennsylvania.</nlm:aff>
<wicri:noCountry code="subfield">Pennsylvania.</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A2">Department of Microbiology and Immunology, MCP Hahnemann University, Philadelphia, Pennsylvania.</nlm:aff>
<wicri:noCountry code="subfield">Pennsylvania.</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A2">Department of Microbiology and Immunology, MCP Hahnemann University, Philadelphia, Pennsylvania.</nlm:aff>
<wicri:noCountry code="subfield">Pennsylvania.</wicri:noCountry>
</affiliation>
Le document en format XML
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Locus Segregates With Diabetes Susceptibility in Congenic WF.<italic>iddm4</italic>
Rats</title>
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<author><name sortKey="Mordes, John P" sort="Mordes, John P" uniqKey="Mordes J" first="John P." last="Mordes">John P. Mordes</name>
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<wicri:noCountry code="subfield">Pennsylvania.</wicri:noCountry>
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<author><name sortKey="Descipio, Cheryl" sort="Descipio, Cheryl" uniqKey="Descipio C" first="Cheryl" last="Descipio">Cheryl Descipio</name>
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<wicri:noCountry code="subfield">Pennsylvania.</wicri:noCountry>
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<series><title level="j">Diabetes</title>
<idno type="ISSN">0012-1797</idno>
<idno type="eISSN">1939-327X</idno>
<imprint><date when="2002">2002</date>
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<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>
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