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LEW.1WR1 RATS DEVELOP AUTOIMMUNE DIABETES SPONTANEOUSLY AND IN RESPONSE TO ENVIRONMENTAL PERTURBATION

Identifieur interne : 000495 ( Pmc/Corpus ); précédent : 000494; suivant : 000496

LEW.1WR1 RATS DEVELOP AUTOIMMUNE DIABETES SPONTANEOUSLY AND IN RESPONSE TO ENVIRONMENTAL PERTURBATION

Auteurs : John P. Mordes ; Dennis L. Guberski ; Jean H. Leif ; Bruce A. Woda ; Joan F. Flanagan ; Dale L. Greiner ; Edward H. Kislauskis ; Rebecca S. Tirabassi

Source :

Diabetes [ 0012-1797 ] ; 2005.

RBID : PMC:1283095

Abstract

We describe a new rat model of autoimmune diabetes that arose in a major histocompatibility complex (MHC) congenic LEW rat. Spontaneous diabetes in LEW.1WR1 rats (RT1^u/u/a) occurs with a cumulative frequency of ∼2% at a median age of 59 days. The disease is characterized by hyperglycemia, glycosuria, ketonuria and polyuria. Both sexes are affected, and islets of acutely diabetic rats are devoid of beta cells whereas alpha and delta cell populations are spared. The peripheral lymphoid phenotype is normal, including the fraction of ART2⁺ regulatory T cells (Tregs). We tested the hypothesis that the expression of diabetes would be increased by immunological perturbation of innate or adaptive immunity. Treatment of young rats with depleting anti-ART2.1 mAb increased the frequency of diabetes to 50%. Treatment with the toll-like receptor 3 (TLR3) ligand polyinosinic:polycytidylic acid increased the frequency of diabetes to 100%. All diabetic rats exhibited end-stage islets. The LEW.1WR1 rat is also susceptible to collagen-induced arthritis but is free of spontaneous thyroiditis. The LEW.1WR1 rat provides a new model for studying autoimmune diabetes and arthritis in an animal with a genetic predisposition to both disorders that can be amplified by environmental perturbation.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1283095

PubMed: 16123363
PubMed Central: 1283095

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PMC:1283095

Le document en format XML

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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>
<affiliation><nlm:aff id="A1">Diabetes Division, Department of Medicine, University of Massachusetts Medical School, Worcester, MA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Guberski, Dennis L" sort="Guberski, Dennis L" uniqKey="Guberski D" first="Dennis L." last="Guberski">Dennis L. Guberski</name>
<affiliation><nlm:aff id="A3">BioMedical Research Models, Inc., Worcester, MA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Leif, Jean H" sort="Leif, Jean H" uniqKey="Leif J" first="Jean H." last="Leif">Jean H. Leif</name>
<affiliation><nlm:aff id="A1">Diabetes Division, Department of Medicine, University of Massachusetts Medical School, Worcester, MA</nlm:aff>
</affiliation>
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<author><name sortKey="Woda, Bruce A" sort="Woda, Bruce A" uniqKey="Woda B" first="Bruce A." last="Woda">Bruce A. Woda</name>
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<author><name sortKey="Flanagan, Joan F" sort="Flanagan, Joan F" uniqKey="Flanagan J" first="Joan F." last="Flanagan">Joan F. Flanagan</name>
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<author><name sortKey="Greiner, Dale L" sort="Greiner, Dale L" uniqKey="Greiner D" first="Dale L." last="Greiner">Dale L. Greiner</name>
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<author><name sortKey="Kislauskis, Edward H" sort="Kislauskis, Edward H" uniqKey="Kislauskis E" first="Edward H." last="Kislauskis">Edward H. Kislauskis</name>
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<author><name sortKey="Tirabassi, Rebecca S" sort="Tirabassi, Rebecca S" uniqKey="Tirabassi R" first="Rebecca S." last="Tirabassi">Rebecca S. Tirabassi</name>
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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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</affiliation>
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<author><name sortKey="Guberski, Dennis L" sort="Guberski, Dennis L" uniqKey="Guberski D" first="Dennis L." last="Guberski">Dennis L. Guberski</name>
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<author><name sortKey="Leif, Jean H" sort="Leif, Jean H" uniqKey="Leif J" first="Jean H." last="Leif">Jean H. Leif</name>
<affiliation><nlm:aff id="A1">Diabetes Division, Department of Medicine, University of Massachusetts Medical School, Worcester, MA</nlm:aff>
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<author><name sortKey="Woda, Bruce A" sort="Woda, Bruce A" uniqKey="Woda B" first="Bruce A." last="Woda">Bruce A. Woda</name>
<affiliation><nlm:aff id="A2">Department of Pathology, University of Massachusetts Medical School, Worcester, MA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Flanagan, Joan F" sort="Flanagan, Joan F" uniqKey="Flanagan J" first="Joan F." last="Flanagan">Joan F. Flanagan</name>
<affiliation><nlm:aff id="A3">BioMedical Research Models, Inc., Worcester, MA</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">Diabetes Division, Department of Medicine, University of Massachusetts Medical School, Worcester, MA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Kislauskis, Edward H" sort="Kislauskis, Edward H" uniqKey="Kislauskis E" first="Edward H." last="Kislauskis">Edward H. Kislauskis</name>
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</affiliation>
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<author><name sortKey="Tirabassi, Rebecca S" sort="Tirabassi, Rebecca S" uniqKey="Tirabassi R" first="Rebecca S." last="Tirabassi">Rebecca S. Tirabassi</name>
<affiliation><nlm:aff id="A3">BioMedical Research Models, Inc., Worcester, MA</nlm:aff>
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<series><title level="j">Diabetes</title>
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<imprint><date when="2005">2005</date>
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<front><div type="abstract" xml:lang="en"><p id="P1">We describe a new rat model of autoimmune diabetes that arose in a major histocompatibility complex (MHC) congenic LEW rat. Spontaneous diabetes in LEW.1WR1 rats (<italic>RT1<sup>u/u/a</sup>
</italic>
) occurs with a cumulative frequency of ∼2% at a median age of 59 days. The disease is characterized by hyperglycemia, glycosuria, ketonuria and polyuria. Both sexes are affected, and islets of acutely diabetic rats are devoid of beta cells whereas alpha and delta cell populations are spared. The peripheral lymphoid phenotype is normal, including the fraction of ART2<sup>+</sup>
 regulatory T cells (Tregs). We tested the hypothesis that the expression of diabetes would be increased by immunological perturbation of innate or adaptive immunity. Treatment of young rats with depleting anti-ART2.1 mAb increased the frequency of diabetes to 50%. Treatment with the toll-like receptor 3 (TLR3) ligand polyinosinic:polycytidylic acid increased the frequency of diabetes to 100%. All diabetic rats exhibited end-stage islets. The LEW.1WR1 rat is also susceptible to collagen-induced arthritis but is free of spontaneous thyroiditis. The LEW.1WR1 rat provides a new model for studying autoimmune diabetes and arthritis in an animal with a genetic predisposition to both disorders that can be amplified by environmental perturbation.</p>
</div>
</front>
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<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-title>Diabetes</journal-title>
<issn pub-type="ppub">0012-1797</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">16123363</article-id>
<article-id pub-id-type="pmc">1283095</article-id>
<article-id pub-id-type="manuscript">NIHMS4640</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>LEW.1WR1 RATS DEVELOP AUTOIMMUNE DIABETES SPONTANEOUSLY AND IN RESPONSE TO ENVIRONMENTAL PERTURBATION</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Mordes</surname>
<given-names>John P.</given-names>
</name>
<degrees>M.D.</degrees>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Guberski</surname>
<given-names>Dennis L.</given-names>
</name>
<degrees>M.S.</degrees>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Leif</surname>
<given-names>Jean H.</given-names>
</name>
<degrees>M.S.</degrees>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Woda</surname>
<given-names>Bruce A.</given-names>
</name>
<degrees>M.D.</degrees>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Flanagan</surname>
<given-names>Joan F.</given-names>
</name>
<degrees>Ph.D.</degrees>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Greiner</surname>
<given-names>Dale L.</given-names>
</name>
<degrees>Ph.D.</degrees>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kislauskis</surname>
<given-names>Edward H.</given-names>
</name>
<degrees>Ph.D.</degrees>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tirabassi</surname>
<given-names>Rebecca S.</given-names>
</name>
<degrees>Ph.D.</degrees>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<aff id="A1"><label>1</label>
Diabetes Division, Department of Medicine, University of Massachusetts Medical School, Worcester, MA</aff>
<aff id="A2"><label>2</label>
Department of Pathology, University of Massachusetts Medical School, Worcester, MA</aff>
<aff id="A3"><label>3</label>
BioMedical Research Models, Inc., Worcester, MA</aff>
</contrib-group>
<author-notes><corresp id="CR1">Address reprint requests to Dennis L. Guberski, BioMedical Research Models Inc, 67 Millbrook St. Worcester, MA 01606</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>17</day>
<month>8</month>
<year>2005</year>
</pub-date>
<pub-date pub-type="ppub"><month>9</month>
<year>2005</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>14</day>
<month>11</month>
<year>2005</year>
</pub-date>
<volume>54</volume>
<issue>9</issue>
<fpage>2727</fpage>
<lpage>2733</lpage>
<abstract><p id="P1">We describe a new rat model of autoimmune diabetes that arose in a major histocompatibility complex (MHC) congenic LEW rat. Spontaneous diabetes in LEW.1WR1 rats (<italic>RT1<sup>u/u/a</sup>
</italic>
) occurs with a cumulative frequency of ∼2% at a median age of 59 days. The disease is characterized by hyperglycemia, glycosuria, ketonuria and polyuria. Both sexes are affected, and islets of acutely diabetic rats are devoid of beta cells whereas alpha and delta cell populations are spared. The peripheral lymphoid phenotype is normal, including the fraction of ART2<sup>+</sup>
 regulatory T cells (Tregs). We tested the hypothesis that the expression of diabetes would be increased by immunological perturbation of innate or adaptive immunity. Treatment of young rats with depleting anti-ART2.1 mAb increased the frequency of diabetes to 50%. Treatment with the toll-like receptor 3 (TLR3) ligand polyinosinic:polycytidylic acid increased the frequency of diabetes to 100%. All diabetic rats exhibited end-stage islets. The LEW.1WR1 rat is also susceptible to collagen-induced arthritis but is free of spontaneous thyroiditis. The LEW.1WR1 rat provides a new model for studying autoimmune diabetes and arthritis in an animal with a genetic predisposition to both disorders that can be amplified by environmental perturbation.</p>
</abstract>
<contract-num rid="DK1">R43 DK060374-01</contract-num>
<contract-num rid="RR1">R41 RR019260-01A1</contract-num>
<contract-sponsor id="DK1">National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK</contract-sponsor>
<contract-sponsor id="RR1">National Center for Research Resources : NCRR</contract-sponsor>
</article-meta>
</front>
</pmc>
</record>

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LEW.1WR1 RATS DEVELOP AUTOIMMUNE DIABETES SPONTANEOUSLY AND IN RESPONSE TO ENVIRONMENTAL PERTURBATION

LEW.1WR1 RATS DEVELOP AUTOIMMUNE DIABETES SPONTANEOUSLY AND IN RESPONSE TO ENVIRONMENTAL PERTURBATION

Source :

Abstract

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