The weak CD8+ CTL response to an influenza hemagglutinin epitope reflects limited T cell availability.
Identifieur interne : 000397 ( PubMed/Corpus ); précédent : 000396; suivant : 000398The weak CD8+ CTL response to an influenza hemagglutinin epitope reflects limited T cell availability.
Auteurs : W. Cao ; B A Myers-Powell ; T J BracialeSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 1996.
English descriptors
- KwdEn :
- Amino Acid Sequence, Animals, Antigen Presentation, Epitopes (immunology), Hemagglutinins, Viral (immunology), Influenza A virus (immunology), Lymphocyte Count, Mice, Mice, Inbred BALB C, Molecular Sequence Data, Multigene Family (immunology), Receptors, Antigen, T-Cell (genetics), T-Lymphocyte Subsets (classification), T-Lymphocyte Subsets (immunology), T-Lymphocytes, Cytotoxic (immunology), Tumor Cells, Cultured.
- MESH :
- chemical , genetics : Receptors, Antigen, T-Cell.
- chemical , immunology : Epitopes, Hemagglutinins, Viral.
- classification : T-Lymphocyte Subsets.
- immunology : Influenza A virus, Multigene Family, T-Lymphocyte Subsets, T-Lymphocytes, Cytotoxic.
- Amino Acid Sequence, Animals, Antigen Presentation, Lymphocyte Count, Mice, Mice, Inbred BALB C, Molecular Sequence Data, Tumor Cells, Cultured.
Abstract
One of the two class I MHC (H-2Kd)-restricted immunogenic regions identified on the influenza virus strain A/Japan/57 (H2N2) hemagglutinin (HA) encompasses two distinct, partially overlapping epitopes. These epitopes map to residues 204 to 212 (JHA 204-212) and 210 to 219 (JHA 210-219), respectively. When we investigated the magnitude of the CTL responses of H-2d BALB/c mice to these two epitopes, we found that the JHA 204-212 nonamer epitope is immunodominant, eliciting vigorous CTL responses in BALB/c mice immunized with A/Japan/57 virus. In contrast, the CTL response to the JHA 210-219 decamer epitope was weak and variable. The subdominance of the JHA 210-219 was not due to low affinity binding of JHA 210-219 to H-2Kd or to inefficient processing of this epitope in vivo. Rather, an analysis of CTL precursor (pCTL) frequency by limiting dilution showed that the frequency of pCTL to the JHA 210-219 epitope was at least 10-fold lower than the frequency of pCTL to the JHA 204-212 epitope, implying that the low and variable response to the JHA 210-219 epitope was due to a limited number of CD8+ T cell precursors directed to JHA 210-219. This hypothesis was further supported by the finding of limited heterogeneity in reactivity pattern displayed by short term bulk cultures of the JHA 210-219-specific CTLs for cross-reactive epitopes. Implications of these findings for vaccine design and for T lymphocyte function and repertoire development are discussed.
PubMed: 8752895
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pubmed:8752895Le document en format XML
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Carter Center for Immunology Research, University of Virginia Health Sciences Center, Charlottesville 22908, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Myers Powell, B A" sort="Myers Powell, B A" uniqKey="Myers Powell B" first="B A" last="Myers-Powell">B A Myers-Powell</name></author><author><name sortKey="Braciale, T J" sort="Braciale, T J" uniqKey="Braciale T" first="T J" last="Braciale">T J Braciale</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1996">1996</date><idno type="RBID">pubmed:8752895</idno><idno type="pmid">8752895</idno><idno type="wicri:Area/PubMed/Corpus">000397</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000397</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The weak CD8+ CTL response to an influenza hemagglutinin epitope reflects limited T cell availability.</title><author><name sortKey="Cao, W" sort="Cao, W" uniqKey="Cao W" first="W" last="Cao">W. Cao</name><affiliation><nlm:affiliation>Beirne B. Carter Center for Immunology Research, University of Virginia Health Sciences Center, Charlottesville 22908, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Myers Powell, B A" sort="Myers Powell, B A" uniqKey="Myers Powell B" first="B A" last="Myers-Powell">B A Myers-Powell</name></author><author><name sortKey="Braciale, T J" sort="Braciale, T J" uniqKey="Braciale T" first="T J" last="Braciale">T J Braciale</name></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="ISSN">0022-1767</idno><imprint><date when="1996" type="published">1996</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Antigen Presentation</term><term>Epitopes (immunology)</term><term>Hemagglutinins, Viral (immunology)</term><term>Influenza A virus (immunology)</term><term>Lymphocyte Count</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Molecular Sequence Data</term><term>Multigene Family (immunology)</term><term>Receptors, Antigen, T-Cell (genetics)</term><term>T-Lymphocyte Subsets (classification)</term><term>T-Lymphocyte Subsets (immunology)</term><term>T-Lymphocytes, Cytotoxic (immunology)</term><term>Tumor Cells, Cultured</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, Antigen, T-Cell</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Epitopes</term><term>Hemagglutinins, Viral</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>T-Lymphocyte Subsets</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Influenza A virus</term><term>Multigene Family</term><term>T-Lymphocyte Subsets</term><term>T-Lymphocytes, Cytotoxic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Antigen Presentation</term><term>Lymphocyte Count</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Molecular Sequence Data</term><term>Tumor Cells, Cultured</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">One of the two class I MHC (H-2Kd)-restricted immunogenic regions identified on the influenza virus strain A/Japan/57 (H2N2) hemagglutinin (HA) encompasses two distinct, partially overlapping epitopes. These epitopes map to residues 204 to 212 (JHA 204-212) and 210 to 219 (JHA 210-219), respectively. When we investigated the magnitude of the CTL responses of H-2d BALB/c mice to these two epitopes, we found that the JHA 204-212 nonamer epitope is immunodominant, eliciting vigorous CTL responses in BALB/c mice immunized with A/Japan/57 virus. In contrast, the CTL response to the JHA 210-219 decamer epitope was weak and variable. The subdominance of the JHA 210-219 was not due to low affinity binding of JHA 210-219 to H-2Kd or to inefficient processing of this epitope in vivo. Rather, an analysis of CTL precursor (pCTL) frequency by limiting dilution showed that the frequency of pCTL to the JHA 210-219 epitope was at least 10-fold lower than the frequency of pCTL to the JHA 204-212 epitope, implying that the low and variable response to the JHA 210-219 epitope was due to a limited number of CD8+ T cell precursors directed to JHA 210-219. This hypothesis was further supported by the finding of limited heterogeneity in reactivity pattern displayed by short term bulk cultures of the JHA 210-219-specific CTLs for cross-reactive epitopes. Implications of these findings for vaccine design and for T lymphocyte function and repertoire development are discussed.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8752895</PMID><DateCompleted><Year>1996</Year><Month>11</Month><Day>07</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-1767</ISSN><JournalIssue CitedMedium="Print"><Volume>157</Volume><Issue>2</Issue><PubDate><Year>1996</Year><Month>Jul</Month><Day>15</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>The weak CD8+ CTL response to an influenza hemagglutinin epitope reflects limited T cell availability.</ArticleTitle><Pagination><MedlinePgn>505-11</MedlinePgn></Pagination><Abstract><AbstractText>One of the two class I MHC (H-2Kd)-restricted immunogenic regions identified on the influenza virus strain A/Japan/57 (H2N2) hemagglutinin (HA) encompasses two distinct, partially overlapping epitopes. These epitopes map to residues 204 to 212 (JHA 204-212) and 210 to 219 (JHA 210-219), respectively. When we investigated the magnitude of the CTL responses of H-2d BALB/c mice to these two epitopes, we found that the JHA 204-212 nonamer epitope is immunodominant, eliciting vigorous CTL responses in BALB/c mice immunized with A/Japan/57 virus. In contrast, the CTL response to the JHA 210-219 decamer epitope was weak and variable. The subdominance of the JHA 210-219 was not due to low affinity binding of JHA 210-219 to H-2Kd or to inefficient processing of this epitope in vivo. Rather, an analysis of CTL precursor (pCTL) frequency by limiting dilution showed that the frequency of pCTL to the JHA 210-219 epitope was at least 10-fold lower than the frequency of pCTL to the JHA 204-212 epitope, implying that the low and variable response to the JHA 210-219 epitope was due to a limited number of CD8+ T cell precursors directed to JHA 210-219. This hypothesis was further supported by the finding of limited heterogeneity in reactivity pattern displayed by short term bulk cultures of the JHA 210-219-specific CTLs for cross-reactive epitopes. Implications of these findings for vaccine design and for T lymphocyte function and repertoire development are discussed.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>W</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Beirne B. Carter Center for Immunology Research, University of Virginia Health Sciences Center, Charlottesville 22908, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Myers-Powell</LastName><ForeName>B A</ForeName><Initials>BA</Initials></Author><Author ValidYN="Y"><LastName>Braciale</LastName><ForeName>T J</ForeName><Initials>TJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Immunol</MedlineTA><NlmUniqueID>2985117R</NlmUniqueID><ISSNLinking>0022-1767</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000939">Epitopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006389">Hemagglutinins, Viral</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011948">Receptors, Antigen, T-Cell</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000595" MajorTopicYN="N">Amino Acid Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017951" MajorTopicYN="N">Antigen Presentation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000939" MajorTopicYN="N">Epitopes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006389" MajorTopicYN="N">Hemagglutinins, Viral</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009980" MajorTopicYN="N">Influenza A virus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018655" MajorTopicYN="N">Lymphocyte Count</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005810" MajorTopicYN="N">Multigene Family</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011948" MajorTopicYN="N">Receptors, Antigen, T-Cell</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016176" MajorTopicYN="N">T-Lymphocyte Subsets</DescriptorName><QualifierName UI="Q000145" MajorTopicYN="N">classification</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013602" MajorTopicYN="N">T-Lymphocytes, Cytotoxic</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014407" MajorTopicYN="N">Tumor Cells, Cultured</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1996</Year><Month>7</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1996</Year><Month>7</Month><Day>15</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1996</Year><Month>7</Month><Day>15</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8752895</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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