Persistence of influenza virus-specific antibody-secreting cells and B-cell memory after primary murine influenza virus infection
Identifieur interne : 002316 ( Main/Exploration ); précédent : 002315; suivant : 002317Persistence of influenza virus-specific antibody-secreting cells and B-cell memory after primary murine influenza virus infection
Auteurs : P. D. Jones [Australie] ; G. L. Ada [Australie]Source :
- Cellular Immunology [ 0008-8749 ] ; 1987.
English descriptors
- Teeft :
- Antigenic stimulation, Ascs, Assay, Cell suspensions, Cell suspensionsobtained, Different subtype, Different subtypes, Different times, Eidso, Eidso afpr8, Germinal centers, Gradual decline, Helper cells, Heterotypic, Heterotypic challenge, Immunization, Indirect elisa, Infectious virus, Influenza, Influenza cells, Influenza infection, Influenza virus, Influenza virus infection, Inoculation, Laboratory mouse, Lung, Lung cell cultures, Lung cell suspensions, Lung virus titers, Memory cells, Monoclonal antibody, Mouse, Peak levels, Primary infection, Primary influenza infection, Primary influenza virus infection, Primary inoculation, Primary lung cell cultures, Respiratory tract, Secondary inoculation, Serum albumin, Significant increase, Small number, Specific ascs, Spleen, Spleen cell cultures, Spleen cell suspensions, Spleen cells, Spleen helper cells, Subsequent decline, Total number, Tracheobronchial washes, Triplicate assaysperformed, Unstimulated cultures, Viral antigens, Virus intranasally, Zmmunol.
Abstract
Abstract: Influenza virus-specific antibody-secreting cells (ASCs), enumerated using an ELISA-plaque assay, were found in the lung and spleen up to 18 months after primary murine influenza infection. The number of ASCs generated in stimulated lung and spleen cell cultures increased 50- to 200-fold after influenza infection. Whereas the level of response did not change in spleen cell cultures up to 18 months after infection, there was a gradual reduction in ASCs in lung cell cultures obtained more than 6 months after infection, predominantly due to a reduction in B memory cells. Homotypic re-infection increased ASCs in the lung only, whereas B-cell memory increased in both the lung and spleen. Although ASCs increased in both the lung and spleen after heterotypic challenge, ASCs and B-cell memory specific for the original subtype were not increased.
Url:
DOI: 10.1016/0008-8749(87)90291-7
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Istex, to step Corpus: 001353
- to stream Istex, to step Curation: 001353
- to stream Istex, to step Checkpoint: 001018
- to stream Main, to step Merge: 002427
- to stream Main, to step Curation: 002316
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Persistence of influenza virus-specific antibody-secreting cells and B-cell memory after primary murine influenza virus infection</title><author><name sortKey="Jones, P D" sort="Jones, P D" uniqKey="Jones P" first="P. D." last="Jones">P. D. Jones</name></author><author><name sortKey="Ada, G L" sort="Ada, G L" uniqKey="Ada G" first="G. L." last="Ada">G. L. Ada</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:49BCEA24FC6723D45ADC7B9132391874EAFE4869</idno><date when="1987" year="1987">1987</date><idno type="doi">10.1016/0008-8749(87)90291-7</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-1PJBSX9W-K/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001353</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001353</idno><idno type="wicri:Area/Istex/Curation">001353</idno><idno type="wicri:Area/Istex/Checkpoint">001018</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">001018</idno><idno type="wicri:doubleKey">0008-8749:1987:Jones P:persistence:of:influenza</idno><idno type="wicri:Area/Main/Merge">002427</idno><idno type="wicri:Area/Main/Curation">002316</idno><idno type="wicri:Area/Main/Exploration">002316</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Persistence of influenza virus-specific antibody-secreting cells and B-cell memory after primary murine influenza virus infection</title><author><name sortKey="Jones, P D" sort="Jones, P D" uniqKey="Jones P" first="P. D." last="Jones">P. D. Jones</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Microbiology, John Curtin School of Medical Research, Australian National University, Canberra, ACT 2601</wicri:regionArea><wicri:noRegion>ACT 2601</wicri:noRegion></affiliation></author><author><name sortKey="Ada, G L" sort="Ada, G L" uniqKey="Ada G" first="G. L." last="Ada">G. L. Ada</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Microbiology, John Curtin School of Medical Research, Australian National University, Canberra, ACT 2601</wicri:regionArea><wicri:noRegion>ACT 2601</wicri:noRegion></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="1987">1987</date><biblScope unit="volume">109</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="53">53</biblScope><biblScope unit="page" to="64">64</biblScope></imprint><idno type="ISSN">0008-8749</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0008-8749</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Antigenic stimulation</term><term>Ascs</term><term>Assay</term><term>Cell suspensions</term><term>Cell suspensionsobtained</term><term>Different subtype</term><term>Different subtypes</term><term>Different times</term><term>Eidso</term><term>Eidso afpr8</term><term>Germinal centers</term><term>Gradual decline</term><term>Helper cells</term><term>Heterotypic</term><term>Heterotypic challenge</term><term>Immunization</term><term>Indirect elisa</term><term>Infectious virus</term><term>Influenza</term><term>Influenza cells</term><term>Influenza infection</term><term>Influenza virus</term><term>Influenza virus infection</term><term>Inoculation</term><term>Laboratory mouse</term><term>Lung</term><term>Lung cell cultures</term><term>Lung cell suspensions</term><term>Lung virus titers</term><term>Memory cells</term><term>Monoclonal antibody</term><term>Mouse</term><term>Peak levels</term><term>Primary infection</term><term>Primary influenza infection</term><term>Primary influenza virus infection</term><term>Primary inoculation</term><term>Primary lung cell cultures</term><term>Respiratory tract</term><term>Secondary inoculation</term><term>Serum albumin</term><term>Significant increase</term><term>Small number</term><term>Specific ascs</term><term>Spleen</term><term>Spleen cell cultures</term><term>Spleen cell suspensions</term><term>Spleen cells</term><term>Spleen helper cells</term><term>Subsequent decline</term><term>Total number</term><term>Tracheobronchial washes</term><term>Triplicate assaysperformed</term><term>Unstimulated cultures</term><term>Viral antigens</term><term>Virus intranasally</term><term>Zmmunol</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Influenza virus-specific antibody-secreting cells (ASCs), enumerated using an ELISA-plaque assay, were found in the lung and spleen up to 18 months after primary murine influenza infection. The number of ASCs generated in stimulated lung and spleen cell cultures increased 50- to 200-fold after influenza infection. Whereas the level of response did not change in spleen cell cultures up to 18 months after infection, there was a gradual reduction in ASCs in lung cell cultures obtained more than 6 months after infection, predominantly due to a reduction in B memory cells. Homotypic re-infection increased ASCs in the lung only, whereas B-cell memory increased in both the lung and spleen. Although ASCs increased in both the lung and spleen after heterotypic challenge, ASCs and B-cell memory specific for the original subtype were not increased.</div></front></TEI><affiliations><list><country><li>Australie</li></country></list><tree><country name="Australie"><noRegion><name sortKey="Jones, P D" sort="Jones, P D" uniqKey="Jones P" first="P. D." last="Jones">P. D. Jones</name></noRegion><name sortKey="Ada, G L" sort="Ada, G L" uniqKey="Ada G" first="G. L." last="Ada">G. L. Ada</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/H2N2V1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002316 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 002316 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= H2N2V1
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:49BCEA24FC6723D45ADC7B9132391874EAFE4869
|texte= Persistence of influenza virus-specific antibody-secreting cells and B-cell memory after primary murine influenza virus infection
}}
| This area was generated with Dilib version V0.6.33. |  |