NOD background genes influence T cell responses to GAD 65 in HLA-DQ8 transgenic mice
Identifieur interne : 003927 ( Main/Exploration ); précédent : 003926; suivant : 003928NOD background genes influence T cell responses to GAD 65 in HLA-DQ8 transgenic mice
Auteurs : Roshini S. Abraham [États-Unis] ; S. Brian Wilson [États-Unis] ; Nelson F. De Souza Jr [États-Unis] ; Jack L. Strominger [États-Unis] ; Stephen R. Munn [Nouvelle-Zélande] ; Chella S. David [États-Unis]Source :
- Human Immunology [ 0198-8859 ] ; 1999.
English descriptors
- KwdEn :
- Teeft :
- American society, Antigen processing, Autoimmune diabetes, Background counts, Background genes, Cell epitopes, Cell repertoire, Cell response, Cell responses, Cryptic epitopes, Decarboxylase, Determinant, Diabetes, Diabetes mellitus, Diabetes patients, Elsevier science, Endogenous class, Epitope, Exogenous antigens, Facs analysis, Flow cytometry, Gene, Glutamic acid decarboxylase, Human immunology, Human type, Immune, Immune response, Immune responses, Immunodominant determinants, Immunodominant epitopes, Immunol, Influence susceptibility, Major histocompatibility, Mayo clinic, Mouse, Mouse class, Peptide, Positive control, Present data, Proc natl acad, Representative experiment, Similar experiments, Strong response, Surface expression, Susceptibility, Transgenic, Transgenic mice.
Abstract
Abstract: The major histocompatibility complex (MHC) genes play a significant role in the predisposition to insulin-dependent diabetes mellitus or type 1 diabetes. HLA-DQ8 (DQB1∗0302, DQA1∗0301) genes have been shown to have the highest relative risk for human type 1 diabetes. To develop a “humanized” mouse model of diabetes, HLA-DQ8 was transgenically expressed in mice lacking endogenous class II genes. Since non-MHC background genes of the NOD influence the disease process, Aβo/DQ8 mice were mated with the NOD strain and backcrossed to generate Aβo/DQ8/NOD mice. These mice have DQ8 as the sole MHC class II restriction element with NOD background genes at the N 2 generation. The DQ8 transgenic mice were used to identify T cell epitopes on glutamic acid decarboxylase (GAD 65), an important putative autoantigen in type 1 diabetes. The NOD background genes strongly influenced antigen processing, that is, different T cell epitopes were generated from the processing of GAD 65 in vivo in the Aβo/DQ8 and in the Aβo/DQ8/NOD mice.
Url:
DOI: 10.1016/S0198-8859(99)00057-9
Affiliations:
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Munn</name><affiliation wicri:level="1"><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Division of Transplant Surgery, Auckland University, Auckland</wicri:regionArea><wicri:noRegion>Auckland</wicri:noRegion></affiliation></author><author><name sortKey="David, Chella S" sort="David, Chella S" uniqKey="David C" first="Chella S" last="David">Chella S. David</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Immunology, Mayo Clinic, Rochester, MN</wicri:regionArea><wicri:noRegion>MN</wicri:noRegion></affiliation><affiliation></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation></author></analytic><monogr></monogr><series><title level="j">Human Immunology</title><title level="j" type="abbrev">HIM</title><idno type="ISSN">0198-8859</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1999">1999</date><biblScope unit="volume">60</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="583">583</biblScope><biblScope unit="page" to="590">590</biblScope></imprint><idno type="ISSN">0198-8859</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0198-8859</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigen processing</term><term>GAD 65</term><term>HLA</term><term>MHC class II</term><term>NOD</term><term>non-MHC genes</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>American society</term><term>Antigen processing</term><term>Autoimmune diabetes</term><term>Background counts</term><term>Background genes</term><term>Cell epitopes</term><term>Cell repertoire</term><term>Cell response</term><term>Cell responses</term><term>Cryptic epitopes</term><term>Decarboxylase</term><term>Determinant</term><term>Diabetes</term><term>Diabetes mellitus</term><term>Diabetes patients</term><term>Elsevier science</term><term>Endogenous class</term><term>Epitope</term><term>Exogenous antigens</term><term>Facs analysis</term><term>Flow cytometry</term><term>Gene</term><term>Glutamic acid decarboxylase</term><term>Human immunology</term><term>Human type</term><term>Immune</term><term>Immune response</term><term>Immune responses</term><term>Immunodominant determinants</term><term>Immunodominant epitopes</term><term>Immunol</term><term>Influence susceptibility</term><term>Major histocompatibility</term><term>Mayo clinic</term><term>Mouse</term><term>Mouse class</term><term>Peptide</term><term>Positive control</term><term>Present data</term><term>Proc natl acad</term><term>Representative experiment</term><term>Similar experiments</term><term>Strong response</term><term>Surface expression</term><term>Susceptibility</term><term>Transgenic</term><term>Transgenic mice</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The major histocompatibility complex (MHC) genes play a significant role in the predisposition to insulin-dependent diabetes mellitus or type 1 diabetes. HLA-DQ8 (DQB1∗0302, DQA1∗0301) genes have been shown to have the highest relative risk for human type 1 diabetes. To develop a “humanized” mouse model of diabetes, HLA-DQ8 was transgenically expressed in mice lacking endogenous class II genes. Since non-MHC background genes of the NOD influence the disease process, Aβo/DQ8 mice were mated with the NOD strain and backcrossed to generate Aβo/DQ8/NOD mice. These mice have DQ8 as the sole MHC class II restriction element with NOD background genes at the N 2 generation. The DQ8 transgenic mice were used to identify T cell epitopes on glutamic acid decarboxylase (GAD 65), an important putative autoantigen in type 1 diabetes. The NOD background genes strongly influenced antigen processing, that is, different T cell epitopes were generated from the processing of GAD 65 in vivo in the Aβo/DQ8 and in the Aβo/DQ8/NOD mice.</div></front></TEI><affiliations><list><country><li>Nouvelle-Zélande</li><li>États-Unis</li></country><region><li>Massachusetts</li></region><settlement><li>Cambridge (Massachusetts)</li></settlement><orgName><li>Université Harvard</li></orgName></list><tree><country name="États-Unis"><noRegion><name sortKey="Abraham, Roshini S" sort="Abraham, Roshini S" uniqKey="Abraham R" first="Roshini S" last="Abraham">Roshini S. Abraham</name></noRegion><name sortKey="David, Chella S" sort="David, Chella S" uniqKey="David C" first="Chella S" last="David">Chella S. David</name><name sortKey="David, Chella S" sort="David, Chella S" uniqKey="David C" first="Chella S" last="David">Chella S. David</name><name sortKey="De Souza Jr, Nelson F" sort="De Souza Jr, Nelson F" uniqKey="De Souza Jr N" first="Nelson F" last="De Souza Jr">Nelson F. De Souza Jr</name><name sortKey="Strominger, Jack L" sort="Strominger, Jack L" uniqKey="Strominger J" first="Jack L" last="Strominger">Jack L. Strominger</name><name sortKey="Wilson, S Brian" sort="Wilson, S Brian" uniqKey="Wilson S" first="S. Brian" last="Wilson">S. Brian Wilson</name></country><country name="Nouvelle-Zélande"><noRegion><name sortKey="Munn, Stephen R" sort="Munn, Stephen R" uniqKey="Munn S" first="Stephen R" last="Munn">Stephen R. Munn</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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