Costimulation by B7 modulates specificity of cytotoxic T lymphocytes: a missing link that explains some bystander T cell activation.
Identifieur interne : 000387 ( PubMed/Corpus ); précédent : 000386; suivant : 000388Costimulation by B7 modulates specificity of cytotoxic T lymphocytes: a missing link that explains some bystander T cell activation.
Auteurs : P. Zheng ; Y. LiuSource :
- The Journal of experimental medicine [ 0022-1007 ] ; 1997.
English descriptors
- KwdEn :
- Animals, Antigens, Viral (immunology), B7-1 Antigen (immunology), Influenza A virus (immunology), Lymphocyte Activation, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Nucleoproteins (immunology), Peptide Fragments (immunology), Receptors, Antigen, T-Cell (immunology), T-Lymphocytes, Cytotoxic (immunology), T-Lymphocytes, Cytotoxic (metabolism), Viral Core Proteins (immunology).
- MESH :
- chemical , immunology : Antigens, Viral, B7-1 Antigen, Nucleoproteins, Peptide Fragments, Receptors, Antigen, T-Cell, Viral Core Proteins.
- immunology : Influenza A virus, T-Lymphocytes, Cytotoxic.
- metabolism : T-Lymphocytes, Cytotoxic.
- Animals, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic.
Abstract
It has been proposed that some bystander T cell activation may in fact be due to T cell antigen receptor (TCR) cross-reactivity that is too low to be detected by the effector cytotoxic T lymphocyte (CTL). However, this hypothesis is not supported by direct evidence since no TCR ligand is known to induce T cell proliferation and differentiation without being recognized by the effector CTL. Here we report that transgenic T cells expressing a T cell receptor to influenza virus A/NT/68 nucleoprotein (NP) 366-374:Db complexes clonally expand and become effector CTLs in response to homologous peptides from either A/PR8/34 (H1N1), A/AA/60 (H2N2), or A/NT/68 (H3N2). However, the effector T cells induced by each of the three peptides kill target cells pulsed with NP peptides from the H3N2 and H2N2 viruses, but not from the H1N1 virus. Thus, NP366-374 from influenza virus H1N1 is the first TCR ligand that can induce T cell proliferation and differentiation without being recognized by CTLs. Since induction of T cell proliferation was mediated by antigen-presenting cells that express costimulatory molecules such as B7, we investigated if cytolysis of H1N1 NP peptide-pulsed targets can be restored by expressing B7-1 on the target cells. Our results revealed that this is the case. These data demonstrated that costimulatory molecule B7 modulates antigen specificity of CTLs, and provides a missing link that explains some of the bystander T cell activation.
DOI: 10.1084/jem.186.10.1787
PubMed: 9362540
Links to Exploration step
pubmed:9362540Le document en format XML
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Liu</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1997">1997</date><idno type="RBID">pubmed:9362540</idno><idno type="pmid">9362540</idno><idno type="doi">10.1084/jem.186.10.1787</idno><idno type="wicri:Area/PubMed/Corpus">000387</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000387</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Costimulation by B7 modulates specificity of cytotoxic T lymphocytes: a missing link that explains some bystander T cell activation.</title><author><name sortKey="Zheng, P" sort="Zheng, P" uniqKey="Zheng P" first="P" last="Zheng">P. Zheng</name><affiliation><nlm:affiliation>Michael Heidelberger Division of Immunology, Department of Pathology, New York University Medical Center 10016, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Y" sort="Liu, Y" uniqKey="Liu Y" first="Y" last="Liu">Y. Liu</name></author></analytic><series><title level="j">The Journal of experimental medicine</title><idno type="ISSN">0022-1007</idno><imprint><date when="1997" type="published">1997</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antigens, Viral (immunology)</term><term>B7-1 Antigen (immunology)</term><term>Influenza A virus (immunology)</term><term>Lymphocyte Activation</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Mice, Transgenic</term><term>Nucleoproteins (immunology)</term><term>Peptide Fragments (immunology)</term><term>Receptors, Antigen, T-Cell (immunology)</term><term>T-Lymphocytes, Cytotoxic (immunology)</term><term>T-Lymphocytes, Cytotoxic (metabolism)</term><term>Viral Core Proteins (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antigens, Viral</term><term>B7-1 Antigen</term><term>Nucleoproteins</term><term>Peptide Fragments</term><term>Receptors, Antigen, T-Cell</term><term>Viral Core Proteins</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Influenza A virus</term><term>T-Lymphocytes, Cytotoxic</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>T-Lymphocytes, Cytotoxic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Lymphocyte Activation</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Mice, Transgenic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It has been proposed that some bystander T cell activation may in fact be due to T cell antigen receptor (TCR) cross-reactivity that is too low to be detected by the effector cytotoxic T lymphocyte (CTL). However, this hypothesis is not supported by direct evidence since no TCR ligand is known to induce T cell proliferation and differentiation without being recognized by the effector CTL. Here we report that transgenic T cells expressing a T cell receptor to influenza virus A/NT/68 nucleoprotein (NP) 366-374:Db complexes clonally expand and become effector CTLs in response to homologous peptides from either A/PR8/34 (H1N1), A/AA/60 (H2N2), or A/NT/68 (H3N2). However, the effector T cells induced by each of the three peptides kill target cells pulsed with NP peptides from the H3N2 and H2N2 viruses, but not from the H1N1 virus. Thus, NP366-374 from influenza virus H1N1 is the first TCR ligand that can induce T cell proliferation and differentiation without being recognized by CTLs. Since induction of T cell proliferation was mediated by antigen-presenting cells that express costimulatory molecules such as B7, we investigated if cytolysis of H1N1 NP peptide-pulsed targets can be restored by expressing B7-1 on the target cells. Our results revealed that this is the case. These data demonstrated that costimulatory molecule B7 modulates antigen specificity of CTLs, and provides a missing link that explains some of the bystander T cell activation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9362540</PMID><DateCompleted><Year>1997</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>08</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-1007</ISSN><JournalIssue CitedMedium="Print"><Volume>186</Volume><Issue>10</Issue><PubDate><Year>1997</Year><Month>Nov</Month><Day>17</Day></PubDate></JournalIssue><Title>The Journal of experimental medicine</Title><ISOAbbreviation>J. Exp. 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However, the effector T cells induced by each of the three peptides kill target cells pulsed with NP peptides from the H3N2 and H2N2 viruses, but not from the H1N1 virus. Thus, NP366-374 from influenza virus H1N1 is the first TCR ligand that can induce T cell proliferation and differentiation without being recognized by CTLs. Since induction of T cell proliferation was mediated by antigen-presenting cells that express costimulatory molecules such as B7, we investigated if cytolysis of H1N1 NP peptide-pulsed targets can be restored by expressing B7-1 on the target cells. Our results revealed that this is the case. 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