Evidence that Th1 Lymphocytes Predominate in Islet Inflammation and Thyroiditis in the BioBreeding (BB) Rat
Identifieur interne : 001A16 ( Main/Exploration ); précédent : 001A15; suivant : 001A17Evidence that Th1 Lymphocytes Predominate in Islet Inflammation and Thyroiditis in the BioBreeding (BB) Rat
Auteurs : Danny Zipris [États-Unis]Source :
- Journal of Autoimmunity [ 0896-8411 ] ; 1996.
English descriptors
- KwdEn :
- Teeft :
- Actin, Additional days, Autoimmune, Autoimmune diabetes, Autoimmunity, Cdna, Cytokine, Cytokine gene expression, Cytokine mrna expression, Diabetes, Diabetic rats, Disease progression, High levels, Iddm, Important role, Islet, Lymphocyte, Mrna, Mrna increase, Pancreatic islets, Rat, Tcrc, Thyroid glands, Thyroiditis, Zipris.
Abstract
Abstract: Th1 cytokines are thought to play a key role in islet inflammation and destruction in insulin-dependent diabetes mellitus (IDDM). We studied this hypothesis in the diabetes-prone (DP)-BB and the diabetes-resistant (DR)-BB rats that are used as a model of human IDDM. The DP-BB rat develops spontaneous autoimmune diabetes at the age of 11–14 weeks. In the DR-BB rat, diabetes is inducible by depletion of RT6+lymphocytes and coadministration of polyinosinic:polycytidylic acid (Poly I:C). We used reverse transcriptase-polymerase chain reaction (RT-PCR) and semi-quantitative PCR techniques to examine mRNA expression of Th1 and Th2 cytokines in inflamed islets and thyroids from DP-BB and DR-BB rats. We observed that in DP-BB and in treated DR-BB rats, the levels of TCRβ, IFN-γ and IL-12p40 mRNA increase with disease progression. In contrast, expression of message for IL-2 and IL-4 is minimal to undetectable in DP-BB and RT6-depleted DR-BB animals at any age. Message for IL-10 is detectable in DP and DR islets; however, its level of expression does not change with disease progression. A similar cytokine mRNA profile is observed in inflamed thyroids from acutely diabetic RT6-depleted DR-BB rats. Incubation of 10wk old DP islets for 48h in the presence of anti-CD3 antibody, followed by an incubation with rIL-2 for an additional 5–7 days, results in an expansion of T lymphocytes, and these cells express high levels of IFN-γ and IL-10 mRNA. Our results suggest that autoimmunity in DP-BB and DR-BB rats is mediated by Th1 lymphocytes and that IFN-γ and IL-12 are likely to play a key role in islet and thyroid inflammation and destruction in IDDM.
Url:
DOI: 10.1006/jaut.1996.0043
Affiliations:
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Evidence that Th1 Lymphocytes Predominate in Islet Inflammation and Thyroiditis in the BioBreeding (BB) Rat</title><author><name sortKey="Zipris, Danny" sort="Zipris, Danny" uniqKey="Zipris D" first="Danny" last="Zipris">Danny Zipris</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:1C13A6D8B00F0920A7CD103DD17E6EE1676F764F</idno><date when="1996" year="1996">1996</date><idno type="doi">10.1006/jaut.1996.0043</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-9GR5S7PD-D/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000433</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000433</idno><idno type="wicri:Area/Istex/Curation">000400</idno><idno type="wicri:Area/Istex/Checkpoint">000428</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">000428</idno><idno type="wicri:doubleKey">0896-8411:1996:Zipris D:evidence:that:th</idno><idno type="wicri:Area/Main/Merge">001A31</idno><idno type="wicri:Area/Main/Curation">001A16</idno><idno type="wicri:Area/Main/Exploration">001A16</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Evidence that Th1 Lymphocytes Predominate in Islet Inflammation and Thyroiditis in the BioBreeding (BB) Rat</title><author><name sortKey="Zipris, Danny" sort="Zipris, Danny" uniqKey="Zipris D" first="Danny" last="Zipris">Danny Zipris</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Diabetes Division, University of Massachusetts Medical Center, Worcester, MA, 01605</wicri:regionArea><wicri:noRegion>01605</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Autoimmunity</title><title level="j" type="abbrev">YJAUT</title><idno type="ISSN">0896-8411</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996">1996</date><biblScope unit="volume">9</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="315">315</biblScope><biblScope unit="page" to="319">319</biblScope></imprint><idno type="ISSN">0896-8411</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0896-8411</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>BB rat</term><term>T lymphocytes</term><term>autoimmune diabetes</term><term>cytokines</term><term>islets</term><term>thyroiditis</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Actin</term><term>Additional days</term><term>Autoimmune</term><term>Autoimmune diabetes</term><term>Autoimmunity</term><term>Cdna</term><term>Cytokine</term><term>Cytokine gene expression</term><term>Cytokine mrna expression</term><term>Diabetes</term><term>Diabetic rats</term><term>Disease progression</term><term>High levels</term><term>Iddm</term><term>Important role</term><term>Islet</term><term>Lymphocyte</term><term>Mrna</term><term>Mrna increase</term><term>Pancreatic islets</term><term>Rat</term><term>Tcrc</term><term>Thyroid glands</term><term>Thyroiditis</term><term>Zipris</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Th1 cytokines are thought to play a key role in islet inflammation and destruction in insulin-dependent diabetes mellitus (IDDM). We studied this hypothesis in the diabetes-prone (DP)-BB and the diabetes-resistant (DR)-BB rats that are used as a model of human IDDM. The DP-BB rat develops spontaneous autoimmune diabetes at the age of 11–14 weeks. In the DR-BB rat, diabetes is inducible by depletion of RT6+lymphocytes and coadministration of polyinosinic:polycytidylic acid (Poly I:C). We used reverse transcriptase-polymerase chain reaction (RT-PCR) and semi-quantitative PCR techniques to examine mRNA expression of Th1 and Th2 cytokines in inflamed islets and thyroids from DP-BB and DR-BB rats. We observed that in DP-BB and in treated DR-BB rats, the levels of TCRβ, IFN-γ and IL-12p40 mRNA increase with disease progression. In contrast, expression of message for IL-2 and IL-4 is minimal to undetectable in DP-BB and RT6-depleted DR-BB animals at any age. Message for IL-10 is detectable in DP and DR islets; however, its level of expression does not change with disease progression. A similar cytokine mRNA profile is observed in inflamed thyroids from acutely diabetic RT6-depleted DR-BB rats. Incubation of 10wk old DP islets for 48h in the presence of anti-CD3 antibody, followed by an incubation with rIL-2 for an additional 5–7 days, results in an expansion of T lymphocytes, and these cells express high levels of IFN-γ and IL-10 mRNA. Our results suggest that autoimmunity in DP-BB and DR-BB rats is mediated by Th1 lymphocytes and that IFN-γ and IL-12 are likely to play a key role in islet and thyroid inflammation and destruction in IDDM.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Zipris, Danny" sort="Zipris, Danny" uniqKey="Zipris D" first="Danny" last="Zipris">Danny Zipris</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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