The immune system response to viral infection of the CNS
Identifieur interne : 000569 ( Istex/Checkpoint ); précédent : 000568; suivant : 000570The immune system response to viral infection of the CNS
Auteurs : Jonathon D. Sedgwick [Allemagne] ; Rüdiger Dörries [Allemagne]Source :
- Seminars in Neuroscience [ 1044-5765 ] ; 1991.
English descriptors
- Teeft :
- Afferent lymphatics, Antigen presentation, Antigen recognition, Blood vessels, Cell receptor, Cerebrospinal fluid, Cervical lymph nodes, Coronavirus demyelinating encephalomyelitis, Cribriform plate, Cytotoxic, Dendritic cells, Endothelial, Endothelial cells, Foreign antigen, High levels, Immune, Immune response, Immune responses, Immune surveillance, Immune system, Immunol, Important role, Infection, Leucocyte, Luminal surface, Lymph, Lymph nodes, Lymphocyte, Major histocompatibility, Mouse hepatitis virus, Node, Possible mechanisms, Present antigen, Same magnification, Vascular endothelium, Viral, Viral clearance, Viral infection, Viral infections, Viral peptides, Virus infection, Visna virus infection.
Abstract
Abstract: In immunological terms the CNS is at a severe disadvantage in its ability to respond to infection by virus. First, both glial and neuronal cells normally do not express molecules of the major histocompatibility complex. Second, the most efficient cells for stimulating an immune response (leucocyte dendritic cells) are not present in the healthy CNS; and third, there is no specialized lymphatic drainage from the CNS to lymph nodes to enable the immune system to be quickly informed of the presence of an infection. Nevertheless, the immune system apparently copes with the vast majority of viral infections in the CNS. This is clearly evidenced by the reactivation of latent CNS viral infections in some immunosuppressed patients and the dramatic increase in the seventy of CNS disease in young or otherwise immunologically incompetent experimental animals infected with neurotropic viruses. The routes by which the CNS and the immune system may communicate and the varied ways in which an immune response may affect the outcome of a viral infection of the CNS are discussed.
Url:
DOI: 10.1016/1044-5765(91)90003-7
Affiliations:
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Sedgwick</name></author><author><name sortKey="Dorries, Rudiger" sort="Dorries, Rudiger" uniqKey="Dorries R" first="Rüdiger" last="Dörries">Rüdiger Dörries</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:7E1B915865C2D00791ECC09D4F28574FF248A10B</idno><date when="1991" year="1991">1991</date><idno type="doi">10.1016/1044-5765(91)90003-7</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-DN3XT6RP-X/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000343</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000343</idno><idno type="wicri:Area/Istex/Curation">000323</idno><idno type="wicri:Area/Istex/Checkpoint">000569</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">000569</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">The immune system response to viral infection of the CNS</title><author><name sortKey="Sedgwick, Jonathon D" sort="Sedgwick, Jonathon D" uniqKey="Sedgwick J" first="Jonathon D." last="Sedgwick">Jonathon D. Sedgwick</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>From the Institute for Virology and Immunobiology, The University of Würzburg, Versbacher Str 7, D-8700 Würzburg</wicri:regionArea><wicri:noRegion>D-8700 Würzburg</wicri:noRegion><wicri:noRegion>D-8700 Würzburg</wicri:noRegion></affiliation></author><author><name sortKey="Dorries, Rudiger" sort="Dorries, Rudiger" uniqKey="Dorries R" first="Rüdiger" last="Dörries">Rüdiger Dörries</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>From the Institute for Virology and Immunobiology, The University of Würzburg, Versbacher Str 7, D-8700 Würzburg</wicri:regionArea><wicri:noRegion>D-8700 Würzburg</wicri:noRegion><wicri:noRegion>D-8700 Würzburg</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Seminars in Neuroscience</title><title level="j" type="abbrev">YSMNS</title><idno type="ISSN">1044-5765</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991">1991</date><biblScope unit="volume">3</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="93">93</biblScope><biblScope unit="page" to="100">100</biblScope></imprint><idno type="ISSN">1044-5765</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1044-5765</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Afferent lymphatics</term><term>Antigen presentation</term><term>Antigen recognition</term><term>Blood vessels</term><term>Cell receptor</term><term>Cerebrospinal fluid</term><term>Cervical lymph nodes</term><term>Coronavirus demyelinating encephalomyelitis</term><term>Cribriform plate</term><term>Cytotoxic</term><term>Dendritic cells</term><term>Endothelial</term><term>Endothelial cells</term><term>Foreign antigen</term><term>High levels</term><term>Immune</term><term>Immune response</term><term>Immune responses</term><term>Immune surveillance</term><term>Immune system</term><term>Immunol</term><term>Important role</term><term>Infection</term><term>Leucocyte</term><term>Luminal surface</term><term>Lymph</term><term>Lymph nodes</term><term>Lymphocyte</term><term>Major histocompatibility</term><term>Mouse hepatitis virus</term><term>Node</term><term>Possible mechanisms</term><term>Present antigen</term><term>Same magnification</term><term>Vascular endothelium</term><term>Viral</term><term>Viral clearance</term><term>Viral infection</term><term>Viral infections</term><term>Viral peptides</term><term>Virus infection</term><term>Visna virus infection</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: In immunological terms the CNS is at a severe disadvantage in its ability to respond to infection by virus. First, both glial and neuronal cells normally do not express molecules of the major histocompatibility complex. Second, the most efficient cells for stimulating an immune response (leucocyte dendritic cells) are not present in the healthy CNS; and third, there is no specialized lymphatic drainage from the CNS to lymph nodes to enable the immune system to be quickly informed of the presence of an infection. Nevertheless, the immune system apparently copes with the vast majority of viral infections in the CNS. This is clearly evidenced by the reactivation of latent CNS viral infections in some immunosuppressed patients and the dramatic increase in the seventy of CNS disease in young or otherwise immunologically incompetent experimental animals infected with neurotropic viruses. The routes by which the CNS and the immune system may communicate and the varied ways in which an immune response may affect the outcome of a viral infection of the CNS are discussed.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country></list><tree><country name="Allemagne"><noRegion><name sortKey="Sedgwick, Jonathon D" sort="Sedgwick, Jonathon D" uniqKey="Sedgwick J" first="Jonathon D." last="Sedgwick">Jonathon D. Sedgwick</name></noRegion><name sortKey="Dorries, Rudiger" sort="Dorries, Rudiger" uniqKey="Dorries R" first="Rüdiger" last="Dörries">Rüdiger Dörries</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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