Costimulation by B7 modulates specificity of cytotoxic T lymphocytes: a missing link that explains some bystander T cell activation.
Identifieur interne : 001353 ( Ncbi/Merge ); précédent : 001352; suivant : 001354Costimulation by B7 modulates specificity of cytotoxic T lymphocytes: a missing link that explains some bystander T cell activation.
Auteurs : P. Zheng [États-Unis] ; Y. LiuSource :
- The Journal of experimental medicine [ 0022-1007 ] ; 1997.
Descripteurs français
- KwdFr :
- Activation des lymphocytes, Animaux, Antigènes viraux (immunologie), Fragments peptidiques (immunologie), Lymphocytes T cytotoxiques (immunologie), Lymphocytes T cytotoxiques (métabolisme), Nucléoprotéines (immunologie), Protéines du core viral (immunologie), Récepteurs aux antigènes des cellules T (immunologie), Souris, Souris de lignée C57BL, Souris knockout, Souris transgéniques, Virus de la grippe A (immunologie).
- MESH :
- immunologie : Antigènes viraux, Fragments peptidiques, Lymphocytes T cytotoxiques, Nucléoprotéines, Protéines du core viral, Récepteurs aux antigènes des cellules T, Virus de la grippe A.
- métabolisme : Lymphocytes T cytotoxiques.
- Activation des lymphocytes, Animaux, Souris, Souris de lignée C57BL, Souris knockout, Souris transgéniques.
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
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pubmed:9362540Le document en format XML
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<term>Lymphocytes T cytotoxiques (immunologie)</term>
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<term>Récepteurs aux antigènes des cellules T (immunologie)</term>
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<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Souris transgéniques</term>
<term>Virus de la grippe A (immunologie)</term>
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<term>Virus de la grippe A</term>
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<term>Animaux</term>
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<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>
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