Characterization of the Acute Immune Response in the Retina of Borna Disease Virus‐infected Lewis Rats
Identifieur interne : 001017 ( Istex/Corpus ); précédent : 001016; suivant : 001018Characterization of the Acute Immune Response in the Retina of Borna Disease Virus‐infected Lewis Rats
Auteurs : T. Stahl ; C. Mohr ; J. Kacza ; T. Pannicke ; S. Sauder ; A. Reichenbach ; J. SeegerSource :
- Anatomia, Histologia, Embryologia [ 0340-2096 ] ; 2005-12.
Abstract
Borna disease virus (BDV) causes a non‐purulent meningoencephalitis and retinitis in a variety of species. In Lewis rats infected intracerebrally with the highly neurotropic BDV the retina is one of the most severely affected central nervous system (CNS) structures. While BDV‐induced damage in the brain has previously been shown to be caused by a T‐cell‐dependent process, the immunopathological mechanisms leading to BDV‐induced retinitis, remain to be elucidated. RNA samples from retinae were subjected to RNase protection assays to detect transcripts of proinflammatory cytokines and chemokines known to be involved in the recruitment of T‐cells and macrophages in the CNS. The observed expression profile of proinflammatory cytokines and chemokines, as well as the immunohistochemical detection of αβTCR‐positive and CD8‐positive T‐cells in the BDV‐infected retinae, is reminiscent of the situation observed in the brains of Lewis rats during the acute phase of Borna disease. This suggests, that similar immunopathological mechanisms are operating in retinae and brains of infected rats. This research was supported by grants from the Deutsche Forschungsgemeinschaft (J.S.‐PA 615/1‐1).
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DOI: 10.1111/j.1439-0264.2005.00669_112.x
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In Lewis rats infected intracerebrally with the highly neurotropic BDV the retina is one of the most severely affected central nervous system (CNS) structures. While BDV‐induced damage in the brain has previously been shown to be caused by a T‐cell‐dependent process, the immunopathological mechanisms leading to BDV‐induced retinitis, remain to be elucidated. RNA samples from retinae were subjected to RNase protection assays to detect transcripts of proinflammatory cytokines and chemokines known to be involved in the recruitment of T‐cells and macrophages in the CNS. The observed expression profile of proinflammatory cytokines and chemokines, as well as the immunohistochemical detection of αβTCR‐positive and CD8‐positive T‐cells in the BDV‐infected retinae, is reminiscent of the situation observed in the brains of Lewis rats during the acute phase of Borna disease. This suggests, that similar immunopathological mechanisms are operating in retinae and brains of infected rats. 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In Lewis rats infected intracerebrally with the highly neurotropic BDV the retina is one of the most severely affected central nervous system (CNS) structures. While BDV‐induced damage in the brain has previously been shown to be caused by a T‐cell‐dependent process, the immunopathological mechanisms leading to BDV‐induced retinitis, remain to be elucidated. RNA samples from retinae were subjected to RNase protection assays to detect transcripts of proinflammatory cytokines and chemokines known to be involved in the recruitment of T‐cells and macrophages in the CNS. The observed expression profile of proinflammatory cytokines and chemokines, as well as the immunohistochemical detection of αβTCR‐positive and CD8‐positive T‐cells in the BDV‐infected retinae, is reminiscent of the situation observed in the brains of Lewis rats during the acute phase of Borna disease. This suggests, that similar immunopathological mechanisms are operating in retinae and brains of infected rats. 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Germany</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Borna disease virus (BDV) causes a non‐purulent meningoencephalitis and retinitis in a variety of species. In Lewis rats infected intracerebrally with the highly neurotropic BDV the retina is one of the most severely affected central nervous system (CNS) structures. While BDV‐induced damage in the brain has previously been shown to be caused by a T‐cell‐dependent process, the immunopathological mechanisms leading to BDV‐induced retinitis, remain to be elucidated. RNA samples from retinae were subjected to RNase protection assays to detect transcripts of proinflammatory cytokines and chemokines known to be involved in the recruitment of T‐cells and macrophages in the CNS. The observed expression profile of proinflammatory cytokines and chemokines, as well as the immunohistochemical detection of αβTCR‐positive and CD8‐positive T‐cells in the BDV‐infected retinae, is reminiscent of the situation observed in the brains of Lewis rats during the acute phase of Borna disease. This suggests, that similar immunopathological mechanisms are operating in retinae and brains of infected rats. This research was supported by grants from the Deutsche Forschungsgemeinschaft (J.S.‐PA 615/1‐1).</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Characterization of the Acute Immune Response in the Retina of Borna Disease Virus‐infected Lewis Rats</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Abstracts</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Characterization of the Acute Immune Response in the Retina of Borna Disease Virus‐infected Lewis Rats</title></titleInfo><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Stahl</namePart><affiliation>Department of Veterinary Anatomy, University of Leipzig, An den Tierkliniken 43, D‐04103 Leipzig</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Mohr</namePart><affiliation>Department of Veterinary Anatomy, University of Leipzig, An den Tierkliniken 43, D‐04103 Leipzig</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Kacza</namePart><affiliation>Department of Veterinary Anatomy, University of Leipzig, An den Tierkliniken 43, D‐04103 Leipzig</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Pannicke</namePart><affiliation>Department of Neurophysiology, Paul Flechsig Institute for Brain Research, University of Leipzig, Jahnallee 59, D‐04109 Leipzig</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Sauder</namePart><affiliation>Department of Virology, Institute for Medical Microbiology and Hygiene, University of Freiburg, Hermann‐Herder‐Straße 11, D‐79008 Freiburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Reichenbach</namePart><affiliation>Department of Neurophysiology, Paul Flechsig Institute for Brain Research, University of Leipzig, Jahnallee 59, D‐04109 Leipzig</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Seeger</namePart><affiliation>Department of Veterinary Anatomy, University of Leipzig, An den Tierkliniken 43, D‐04103 Leipzig</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="abstract" displayLabel="abstract"></genre><originInfo><publisher>Blackwell Verlag GmbH</publisher><place><placeTerm type="text">Berlin, Germany</placeTerm></place><dateIssued encoding="w3cdtf">2005-12</dateIssued><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Borna disease virus (BDV) causes a non‐purulent meningoencephalitis and retinitis in a variety of species. In Lewis rats infected intracerebrally with the highly neurotropic BDV the retina is one of the most severely affected central nervous system (CNS) structures. While BDV‐induced damage in the brain has previously been shown to be caused by a T‐cell‐dependent process, the immunopathological mechanisms leading to BDV‐induced retinitis, remain to be elucidated. RNA samples from retinae were subjected to RNase protection assays to detect transcripts of proinflammatory cytokines and chemokines known to be involved in the recruitment of T‐cells and macrophages in the CNS. The observed expression profile of proinflammatory cytokines and chemokines, as well as the immunohistochemical detection of αβTCR‐positive and CD8‐positive T‐cells in the BDV‐infected retinae, is reminiscent of the situation observed in the brains of Lewis rats during the acute phase of Borna disease. This suggests, that similar immunopathological mechanisms are operating in retinae and brains of infected rats. This research was supported by grants from the Deutsche Forschungsgemeinschaft (J.S.‐PA 615/1‐1).</abstract><relatedItem type="host"><titleInfo><title>Anatomia, Histologia, Embryologia</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0340-2096</identifier><identifier type="eISSN">1439-0264</identifier><identifier type="DOI">10.1111/(ISSN)1439-0264</identifier><identifier type="PublisherID">AHE</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>34</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>s1</number></detail><extent unit="pages"><start>49</start><end>49</end></extent></part></relatedItem><identifier type="istex">D750A3CBC62348B3B39FAE56471E2A47D48A81C0</identifier><identifier type="DOI">10.1111/j.1439-0264.2005.00669_112.x</identifier><identifier type="ArticleID">AHE669_112_112</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Verlag GmbH</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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