The RT6 Rat Lymphocyte Alloantigen Circulates in Soluble Form
Identifieur interne : 001A99 ( Main/Exploration ); précédent : 001A98; suivant : 001B00The RT6 Rat Lymphocyte Alloantigen Circulates in Soluble Form
Auteurs : Debra J. Waite [États-Unis] ; Eugene S. Handler [États-Unis] ; John P. Mordes [États-Unis] ; Aldo A. Rossini [États-Unis] ; Dale L. Greiner [États-Unis]Source :
- Cellular Immunology [ 0008-8749 ] ; 1993.
Abstract
Abstract: RT6 is a rat maturational lymphocyte alloantigen that appears to subserve important immunoregulatory functions. The lymphopenic diabetes-prone BioBreeding (BB)/Worcester rat is severely deficient in RT6+ T cells and develops spontaneous autoimmune diabetes mellitus. Transfusion of RT6+ T cells prevents the disease. Conversely, in vivo immune elimination of RT6+ T cells from the diabetes-resistant line of BB rats induces diabetes and thyroiditis. RT6 protein is expressed in two allotypic forms, each linked to the cell surface by a phosphatidylinositol (PI) anchor. The mechanism by which RT6+ T cells exert their regulatory function is not known, nor is the function of the RT6 protein defined. In this study, we investigated the possibility that, like other PI-linked proteins. RT6 also exists in a soluble from in the circulation. Using standard biochemical procedures we observed: (i) Soluble RT6 circulates in readily detectable amounts in all rat strains studied. (ii) The diabetes-prone BB rat circulates less RT6.1 than does any other strain, including the coisogenic diabetes-resistant line. (iii) Injections of monoclonal anti-RT6.1 antibody rapidly eliminate soluble RT6 from the circulation of diabetes resistant BB rats. The existence of a soluble form of a protein associated with immunoregulatory T cells suggests the possibility that soluble RT6 itself might possess immunomodulatory properties.
Url:
DOI: 10.1006/cimm.1993.1269
Affiliations:
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Waite</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Department of Medicine, University of Massachusetts Medical School, Worcester</wicri:cityArea></affiliation></author><author><name sortKey="Handler, Eugene S" sort="Handler, Eugene S" uniqKey="Handler E" first="Eugene S." last="Handler">Eugene S. Handler</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Department of Medicine, University of Massachusetts Medical School, Worcester</wicri:cityArea></affiliation></author><author><name sortKey="Mordes, John P" sort="Mordes, John P" uniqKey="Mordes J" first="John P." last="Mordes">John P. 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Greiner</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Department of Medicine, University of Massachusetts Medical School, Worcester</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Cellular Immunology</title><title level="j" type="abbrev">YCIMM</title><idno type="ISSN">0008-8749</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993">1993</date><biblScope unit="volume">152</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="82">82</biblScope><biblScope unit="page" to="95">95</biblScope></imprint><idno type="ISSN">0008-8749</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0008-8749</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: RT6 is a rat maturational lymphocyte alloantigen that appears to subserve important immunoregulatory functions. The lymphopenic diabetes-prone BioBreeding (BB)/Worcester rat is severely deficient in RT6+ T cells and develops spontaneous autoimmune diabetes mellitus. Transfusion of RT6+ T cells prevents the disease. Conversely, in vivo immune elimination of RT6+ T cells from the diabetes-resistant line of BB rats induces diabetes and thyroiditis. RT6 protein is expressed in two allotypic forms, each linked to the cell surface by a phosphatidylinositol (PI) anchor. The mechanism by which RT6+ T cells exert their regulatory function is not known, nor is the function of the RT6 protein defined. In this study, we investigated the possibility that, like other PI-linked proteins. RT6 also exists in a soluble from in the circulation. Using standard biochemical procedures we observed: (i) Soluble RT6 circulates in readily detectable amounts in all rat strains studied. (ii) The diabetes-prone BB rat circulates less RT6.1 than does any other strain, including the coisogenic diabetes-resistant line. (iii) Injections of monoclonal anti-RT6.1 antibody rapidly eliminate soluble RT6 from the circulation of diabetes resistant BB rats. The existence of a soluble form of a protein associated with immunoregulatory T cells suggests the possibility that soluble RT6 itself might possess immunomodulatory properties.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li></region></list><tree><country name="États-Unis"><region name="Massachusetts"><name sortKey="Waite, Debra J" sort="Waite, Debra J" uniqKey="Waite D" first="Debra J." last="Waite">Debra J. Waite</name></region><name sortKey="Greiner, Dale L" sort="Greiner, Dale L" uniqKey="Greiner D" first="Dale L." last="Greiner">Dale L. Greiner</name><name sortKey="Handler, Eugene S" sort="Handler, Eugene S" uniqKey="Handler E" first="Eugene S." last="Handler">Eugene S. Handler</name><name sortKey="Mordes, John P" sort="Mordes, John P" uniqKey="Mordes J" first="John P." last="Mordes">John P. Mordes</name><name sortKey="Rossini, Aldo A" sort="Rossini, Aldo A" uniqKey="Rossini A" first="Aldo A." last="Rossini">Aldo A. Rossini</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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