The RT6 Rat Lymphocyte Alloantigen Circulates in Soluble Form
Identifieur interne : 000799 ( Istex/Corpus ); précédent : 000798; suivant : 000800The RT6 Rat Lymphocyte Alloantigen Circulates in Soluble Form
Auteurs : Debra J. Waite ; Eugene S. Handler ; John P. Mordes ; Aldo A. Rossini ; Dale L. GreinerSource :
- 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
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Waite</name><affiliation><mods:affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</mods:affiliation></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><mods:affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</mods:affiliation></affiliation></author><author><name sortKey="Mordes, John P" sort="Mordes, John P" uniqKey="Mordes J" first="John P." last="Mordes">John P. Mordes</name><affiliation><mods:affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</mods:affiliation></affiliation></author><author><name sortKey="Rossini, Aldo A" sort="Rossini, Aldo A" uniqKey="Rossini A" first="Aldo A." last="Rossini">Aldo A. 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Greiner</name><affiliation><mods:affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</mods:affiliation></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><istex><corpusName>elsevier</corpusName><author><json:item><name>Debra J. Waite</name><affiliations><json:string>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</json:string></affiliations></json:item><json:item><name>Eugene S. Handler</name><affiliations><json:string>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</json:string></affiliations></json:item><json:item><name>John P. Mordes</name><affiliations><json:string>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</json:string></affiliations></json:item><json:item><name>Aldo A. Rossini</name><affiliations><json:string>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</json:string></affiliations></json:item><json:item><name>Dale L. Greiner</name><affiliations><json:string>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</json:string></affiliations></json:item></author><articleId><json:string>71269</json:string></articleId><arkIstex>ark:/67375/6H6-66MVNGVR-N</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><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. 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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.</p></abstract></profileDesc><revisionDesc><change when="1993">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-66MVNGVR-N/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier converted-article found"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>YCIMM</jid><aid>71269</aid><ce:pii>S0008-8749(83)71269-4</ce:pii><ce:doi>10.1006/cimm.1993.1269</ce:doi><ce:copyright type="full-transfer" year="1993">Academic Press</ce:copyright></item-info><head><ce:dochead><ce:textfn>Regular Article</ce:textfn></ce:dochead><ce:title>The RT6 Rat Lymphocyte Alloantigen Circulates in Soluble Form</ce:title><ce:author-group><ce:author><ce:given-name>Debra J.</ce:given-name><ce:surname>Waite</ce:surname></ce:author><ce:author><ce:given-name>Eugene S.</ce:given-name><ce:surname>Handler</ce:surname></ce:author><ce:author><ce:given-name>John P.</ce:given-name><ce:surname>Mordes</ce:surname></ce:author><ce:author><ce:given-name>Aldo A.</ce:given-name><ce:surname>Rossini</ce:surname></ce:author><ce:author><ce:given-name>Dale L.</ce:given-name><ce:surname>Greiner</ce:surname></ce:author><ce:affiliation><ce:textfn>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</ce:textfn></ce:affiliation></ce:author-group><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">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<ce:sup loc="post">+</ce:sup> T cells and develops spontaneous autoimmune diabetes mellitus. Transfusion of RT6<ce:sup loc="post">+</ce:sup> T cells prevents the disease. Conversely, <ce:italic>in vivo</ce:italic> immune elimination of RT6<ce:sup loc="post">+</ce:sup> 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<ce:sup loc="post">+</ce:sup> 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.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The RT6 Rat Lymphocyte Alloantigen Circulates in Soluble Form</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>The RT6 Rat Lymphocyte Alloantigen Circulates in Soluble Form</title></titleInfo><name type="personal"><namePart type="given">Debra J.</namePart><namePart type="family">Waite</namePart><affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eugene S.</namePart><namePart type="family">Handler</namePart><affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John P.</namePart><namePart type="family">Mordes</namePart><affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Aldo A.</namePart><namePart type="family">Rossini</namePart><affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dale L.</namePart><namePart type="family">Greiner</namePart><affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1993</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract 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. 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