RapamycinFungusV1, Main, Exploration, bibRecord, 001371

When Toll-like receptor and T-cell receptor signals collide: a mechanism for enhanced CD8 T-cell effector function.

Identifieur interne : 001371 ( Main/Exploration ); précédent : 001370; suivant : 001372

When Toll-like receptor and T-cell receptor signals collide: a mechanism for enhanced CD8 T-cell effector function.

Auteurs : Degui Geng [États-Unis] ; Liqin Zheng ; Ratika Srivastava ; Nicole Asprodites ; Cruz Velasco-Gonzalez ; Eduardo Davila

Source :

Blood [ 1528-0020 ] ; 2010.

RBID : pubmed:20696947

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), CD8-Positive T-Lymphocytes (immunology), CD8-Positive T-Lymphocytes (microbiology), Gene Expression Regulation (MeSH), Granzymes (immunology), Interferon-gamma (genetics), Interferon-gamma (immunology), Mice (MeSH), Myeloid Differentiation Factor 88 (immunology), Perforin (genetics), Perforin (immunology), Phosphatidylinositol 3-Kinases (immunology), Phosphoinositide-3 Kinase Inhibitors (MeSH), Protein Kinase C (antagonists & inhibitors), Protein Kinase C (immunology), Receptors, Antigen, T-Cell (immunology), T-Box Domain Proteins (genetics), T-Box Domain Proteins (immunology), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (immunology), Toll-Like Receptor 2 (immunology), Toll-Like Receptors (immunology).
MESH :
- chemical , antagonists & inhibitors : Protein Kinase C, TOR Serine-Threonine Kinases.
- chemical , genetics : Interferon-gamma, Perforin, T-Box Domain Proteins.
- chemical , immunology : Granzymes, Interferon-gamma, Myeloid Differentiation Factor 88, Perforin, Protein Kinase C, Receptors, Antigen, T-Cell, T-Box Domain Proteins, TOR Serine-Threonine Kinases, Toll-Like Receptor 2, Toll-Like Receptors.
- immunology : CD8-Positive T-Lymphocytes, Phosphatidylinositol 3-Kinases.
- microbiology : CD8-Positive T-Lymphocytes.
- Animals, Gene Expression Regulation, Mice, Phosphoinositide-3 Kinase Inhibitors.

Abstract

Emerging reports reveal that activating Toll-like receptor-2 (TLR2)-MyD88 signals in CD8 T lymphocytes enhances cytokine production and cytotoxicity; however, the signaling pathway remains undefined. In the present study, we examined the physiologic significance and molecular mechanisms involved in this process. We found that TLR2 engagement on T-cell receptor transgenic CD8 OT-1 T cells increased T-bet transcription factor levels consequently, augmenting effector transcript and protein levels both in vivo and in vitro. In contrast, TLR2 agonist did not costimulate TLR2(-/-)OT-1 or MyD88(-/-)OT-1 T cells. Elevated T-bet levels in TLR2-MyD88-activated T cells was a consequence of increased biosynthesis resulting from the enhanced activation of the mammalian target of the rapamycin (mTOR) pathway. Inhibiting mTOR, Akt, or protein kinase C in T cells abolished the costimulatory effects of the TLR2 agonist. In vivo, activating TLR2-MyD88 signals in T cells increased effector-molecule levels and enhanced the clearance of Listeria monocytogenes-Ova. These results help define a signaling pathway linking the TLR-MyD88 and mTOR pathway in an Akt- and protein kinase C-dependent manner. These results highlight a critical role for MyD88 signaling in T-cell activation and cytotoxicity. Furthermore, these findings offer the opportunity for improving the efficacy of vaccines and T cell-based immunotherapies by targeting TLR-MyD88 signaling within T cells.

DOI: 10.1182/blood-2010-02-268169
PubMed: 20696947
PubMed Central: PMC2981476

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 001383
to stream Main, to step Curation: 001383

Le document en format XML

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<term>CD8-Positive T-Lymphocytes (immunology)</term>
<term>CD8-Positive T-Lymphocytes (microbiology)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Granzymes (immunology)</term>
<term>Interferon-gamma (genetics)</term>
<term>Interferon-gamma (immunology)</term>
<term>Mice (MeSH)</term>
<term>Myeloid Differentiation Factor 88 (immunology)</term>
<term>Perforin (genetics)</term>
<term>Perforin (immunology)</term>
<term>Phosphatidylinositol 3-Kinases (immunology)</term>
<term>Phosphoinositide-3 Kinase Inhibitors (MeSH)</term>
<term>Protein Kinase C (antagonists & inhibitors)</term>
<term>Protein Kinase C (immunology)</term>
<term>Receptors, Antigen, T-Cell (immunology)</term>
<term>T-Box Domain Proteins (genetics)</term>
<term>T-Box Domain Proteins (immunology)</term>
<term>TOR Serine-Threonine Kinases (antagonists & inhibitors)</term>
<term>TOR Serine-Threonine Kinases (immunology)</term>
<term>Toll-Like Receptor 2 (immunology)</term>
<term>Toll-Like Receptors (immunology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Facteur de différenciation myéloïde-88 (immunologie)</term>
<term>Granzymes (immunologie)</term>
<term>Interféron gamma (génétique)</term>
<term>Interféron gamma (immunologie)</term>
<term>Lymphocytes T CD8+ (immunologie)</term>
<term>Lymphocytes T CD8+ (microbiologie)</term>
<term>Perforine (génétique)</term>
<term>Perforine (immunologie)</term>
<term>Phosphatidylinositol 3-kinases (immunologie)</term>
<term>Protéine kinase C (antagonistes et inhibiteurs)</term>
<term>Protéine kinase C (immunologie)</term>
<term>Protéines à domaine boîte-T (génétique)</term>
<term>Protéines à domaine boîte-T (immunologie)</term>
<term>Récepteur de type Toll-2 (immunologie)</term>
<term>Récepteurs aux antigènes des cellules T (immunologie)</term>
<term>Récepteurs de type Toll (immunologie)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Souris (MeSH)</term>
<term>Sérine-thréonine kinases TOR (antagonistes et inhibiteurs)</term>
<term>Sérine-thréonine kinases TOR (immunologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Protein Kinase C</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interferon-gamma</term>
<term>Perforin</term>
<term>T-Box Domain Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Granzymes</term>
<term>Interferon-gamma</term>
<term>Myeloid Differentiation Factor 88</term>
<term>Perforin</term>
<term>Protein Kinase C</term>
<term>Receptors, Antigen, T-Cell</term>
<term>T-Box Domain Proteins</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Toll-Like Receptor 2</term>
<term>Toll-Like Receptors</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéine kinase C</term>
<term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Interféron gamma</term>
<term>Perforine</term>
<term>Protéines à domaine boîte-T</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Facteur de différenciation myéloïde-88</term>
<term>Granzymes</term>
<term>Interféron gamma</term>
<term>Lymphocytes T CD8+</term>
<term>Perforine</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéine kinase C</term>
<term>Protéines à domaine boîte-T</term>
<term>Récepteur de type Toll-2</term>
<term>Récepteurs aux antigènes des cellules T</term>
<term>Récepteurs de type Toll</term>
<term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term>
<term>Phosphatidylinositol 3-Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Lymphocytes T CD8+</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Gene Expression Regulation</term>
<term>Mice</term>
<term>Phosphoinositide-3 Kinase Inhibitors</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Régulation de l'expression des gènes</term>
<term>Souris</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Emerging reports reveal that activating Toll-like receptor-2 (TLR2)-MyD88 signals in CD8 T lymphocytes enhances cytokine production and cytotoxicity; however, the signaling pathway remains undefined. In the present study, we examined the physiologic significance and molecular mechanisms involved in this process. We found that TLR2 engagement on T-cell receptor transgenic CD8 OT-1 T cells increased T-bet transcription factor levels consequently, augmenting effector transcript and protein levels both in vivo and in vitro. In contrast, TLR2 agonist did not costimulate TLR2(-/-)OT-1 or MyD88(-/-)OT-1 T cells. Elevated T-bet levels in TLR2-MyD88-activated T cells was a consequence of increased biosynthesis resulting from the enhanced activation of the mammalian target of the rapamycin (mTOR) pathway. Inhibiting mTOR, Akt, or protein kinase C in T cells abolished the costimulatory effects of the TLR2 agonist. In vivo, activating TLR2-MyD88 signals in T cells increased effector-molecule levels and enhanced the clearance of Listeria monocytogenes-Ova. These results help define a signaling pathway linking the TLR-MyD88 and mTOR pathway in an Akt- and protein kinase C-dependent manner. These results highlight a critical role for MyD88 signaling in T-cell activation and cytotoxicity. Furthermore, these findings offer the opportunity for improving the efficacy of vaccines and T cell-based immunotherapies by targeting TLR-MyD88 signaling within T cells.</div>
</front>
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<Abstract><AbstractText>Emerging reports reveal that activating Toll-like receptor-2 (TLR2)-MyD88 signals in CD8 T lymphocytes enhances cytokine production and cytotoxicity; however, the signaling pathway remains undefined. In the present study, we examined the physiologic significance and molecular mechanisms involved in this process. We found that TLR2 engagement on T-cell receptor transgenic CD8 OT-1 T cells increased T-bet transcription factor levels consequently, augmenting effector transcript and protein levels both in vivo and in vitro. In contrast, TLR2 agonist did not costimulate TLR2(-/-)OT-1 or MyD88(-/-)OT-1 T cells. Elevated T-bet levels in TLR2-MyD88-activated T cells was a consequence of increased biosynthesis resulting from the enhanced activation of the mammalian target of the rapamycin (mTOR) pathway. Inhibiting mTOR, Akt, or protein kinase C in T cells abolished the costimulatory effects of the TLR2 agonist. In vivo, activating TLR2-MyD88 signals in T cells increased effector-molecule levels and enhanced the clearance of Listeria monocytogenes-Ova. These results help define a signaling pathway linking the TLR-MyD88 and mTOR pathway in an Akt- and protein kinase C-dependent manner. These results highlight a critical role for MyD88 signaling in T-cell activation and cytotoxicity. Furthermore, these findings offer the opportunity for improving the efficacy of vaccines and T cell-based immunotherapies by targeting TLR-MyD88 signaling within T cells.</AbstractText>
</Abstract>
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<ForeName>Degui</ForeName>
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</AffiliationInfo>
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	Serveur d'exploration sur la rapamycine et les champignons
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When Toll-like receptor and T-cell receptor signals collide: a mechanism for enhanced CD8 T-cell effector function.

When Toll-like receptor and T-cell receptor signals collide: a mechanism for enhanced CD8 T-cell effector function.

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